PvM posted Entry 2006 on February 13, 2006 10:00 AM.
Trackback URL: http://www.pandasthumb.org/cgi-bin/mt/mt-tb.fcgi/2001

A while ago on ASA, Glenn Morton referenced the work by Boraas. I have always been fascinated by this reference but unable to find much relevant literature. Until recently, when I accidentally ran across more recent reearch in this area. I would like to share what I learned and how these findings may help understand evolution of multicellularity.

The original references was to a paper published in EOS called “Predator-mediated algal evolution in Chemostat culture”. In 1998, Boraas published another paper titled “Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity” in Evolutionary Ecology 1998, 12, 153-164

According to the original abstract, an unknown predator had invaded a chemostat containing algae. While many of the algae fell prey to the predator, a news species arose consisting of clusters of multiple cells. This seems the first logical step towards full multi-cellularity where cells take on specific roles.

The original abstract reads

An unidentified microflagellate specie (4-12 [mico]m) and Chlorella Prenodosa (2-5 [micro]m) were grown at 25 C in mixed-species chemostats with constant light and sterile, inorganic medium flow. The flagellate readily consumed the algae and grew rapidly (doubling time ca. 6 h). Size distributions of both species are shown in the Figure (area = biovolume). After an initial oscillation (curves 1,2), the system apparently stabilized with both species coexisting. The algal population now consisted of clusters of 4 to tens of cells that were immune to predation by the flagellate (curve 3). The mean cluster size then steadily decreased (curve 4) and stabilized at 4-8 cells (curve 5). These, and other, observations support the hypothesis: (1) a multicellular algal form was selected as a response to predation pressures, (2) a minimum cluster size was selected due to nutrient competition (large clusters have a smaller surface area per unite biomass) and (3) genetic, morphological, and structural diversity of the system increased as a response to predation. Flagellate predation influences both the genetics and the dynamics of microalgal population.”

the 1998 paper reports on experiments with predation

Summary

Predation was a powerful selective force promoting increased morphological complexity in a unicellular prey held in constant environmental conditions. The green alga, Chlorella vulgaris, is a well-studied eukaryote, which has retained its normal unicellular form in cultures in our laboratories for thousands of generations. For the experiments reported here, steady-state unicellular C. vulgaris continuous cultures were inoculated with the predator Ochromonas vallescia, a phagotrophic flagellated protist (‘flagellate’). Within less than 100 generations of the prey, a multicellular Chlorella growth form became dominant in the culture (subsequently repeated in other cultures). The prey Chlorella first formed globose clusters of tens to hundreds of cells. After about 10-20 generations in the presence of the phagotroph, eight-celled colonies predominated. These colonies retained the eight-celled form indefinitely in continuous culture and when plated onto agar. These self-replicating, stable colonies were virtually immune to predation by the flagellate, but small enough that each Chlorella cell was exposed directly to the nutrient medium.

The article showed how when a common uni-celllular alga “Chlorella vulgaris” was exposed to a predator “Ochromonas vellesiaca”, a phagotrophic flagellate, within 100 generations or so, a multicellular (colonial) specie arose .

The results were discussed in a 2000 TalkOrigins Post of the Month by Adam Noel Harris and in TalkOrigin’s Index to Creationist Claims CB904

In other words, the innovsative step from single to multi-cellular may well have taken place under selective pressures of predation. The work by Boraas shows that even accidents such as allowing predators iside chemostats can lead through hard work to fascinating new scientific findings and insights.

The authors mention that other than in rare instances, the Chlorella culture had always exhibitied its normal unicellular morphology over a timeframe of 2 decades.

When the predator was introduced, predictably the prey density declined and the predator density increased. When the predators started to run out of food, they started to decline and the reduction in predation led to a recovery of the Chlorella population (this is a classical pre-predator interaction). During the recovery phase, it was noticed that in addition to unicellular forms, there now existed colonial forms with the numbers of cells ranging from four to hundreds. Eventually the system entered a steady state with the Chlorella population consisting of colonies of 8 cells. These colonies were not only stable but also self-replicating

The authors conclude that the muli-cellular form is a rare mutation which was selected by predation and thus ‘amplified’. The authors also discuss the issue of induction, namely that the flagellates released a substance that caused colony formation. Given that it took almost 20 generations before colonies became apparant, the authors reject this alternative. Additionally, multicellular colonies were maintained even in low density cultures and finally, when the colonies are allowed to reproduce by themselves, they reproduce as colonies not single cells. The authors finally show how these experiments support a thesis by Stanley that multicellular life arose late into the pre-Cambrian under selective pressure of predation.
Was the Cambrian explosion in other words, an arms race between prey and predator?

That under selective pressure, mulicellular colonies arose, shows how the simple processes of variation and selection can surely explain innovation and increase in complexity.

Stanley, S.M. (1973) An ecological theory for the sudden origin of multicellular life in the Late Precambrian PNAS 70, 1486-1489.

According to modern ecological theory, high diversity at any trophic level of a community is possible only under the influence of cropping. Until herbivores evolved, single-celled algae of the Precambrian were resource-limited, and a small number of species saturated aquatic environments. In the near-absence of vacant niches, life diversified slowly. Because the changes required to produce the first algae-eating heterotrophs were therefore delayed, the entire system was self-limiting. When the “heterotroph barrier” was finally crossed in the late Precambrian, herbivorous and carnivorous protists arose almost simultaneously, for no major biological differences separate the two groups. These events automatically triggered the formation of a series of self-propagating feedback systems of diversification between adjacent trophic levels. Comparable systems arose among multicellular groups, which radiated rapidly from the newly diversifying protist taxa. The sudden proliferation of complex food webs formed by taxa invading previously vacant adaptive zones produced an explosive diversification of life over a period of a few tens of millions of years. The rapid appearance of skeletons in various groups, though of special geological importance, was no more dramatic than other aspects of the radiation. The overall rate of diversification was comparable to rates for less-extensive adaptive radiations of the Phanerozoic.

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Comment #79500

Posted by Henry J on February 13, 2006 4:43 PM (e)

Re “Was the Cambrian explosion in other words, an arms race between prey and predator?”

Fascinating!

Comment #79511

Posted by qetzal on February 13, 2006 5:17 PM (e)

Great post and great topic!

Question - anyone know any good research on why multicellular organisms are almost all eukaryotic?

Comment #79529

Posted by PvM on February 13, 2006 6:23 PM (e)

Another green Algae also provide a nice example as to how sex may have evolved (Andy/Larry? are you listening?)
From this link we learn that chlamydomonas divides both sexually and asexually. Sexual reproduction is stimulated by environmental stress.

Many features of chlamydomonas sex are believed to have evolved early in the chlorophyte lineage. Using this basic life cycle, many refinements that evolved among the chlorophytes have been identified.

  1. Some green algae produce gametes that differ from vegetative cells, and in some species, the male gamete differs in size or morphology from the female gamete (anisogamy)
  2. Many species exhibit oogamy, a type of anosogamy in which a flagellated sperm fertilizes a nonmotile egg.
  3. Some multicellular species also exhibit alternation of generations
  4. Ulva produces isomorphic thalli for its diploid sporophyte and haploid gametophyte.

From isogamy where both “egg” and “sperm” are one and the same, to anisogamy where the egg hecomes the larger and the sperm the smaller one to oogamy where the sperm is now flagellated and fertilizes an egg with no flagella.

Cool stuff

Comment #79530

Posted by PvM on February 13, 2006 6:24 PM (e)

Using these relatively simple organisms, we can ‘re-create’ plausible pathways for the evolution of multi-cellularity, the evolution of sex and the evolution of diversification. Not bad

Comment #79599

Posted by Bruce Thompson GQ on February 13, 2006 10:36 PM (e)

This would appear to be analogous to recent events at
Uncommonly Decent. The Blog has become multi-cellular but in addition displays cellular specializations. The appointment of a Blog Czar with online banning and censorship powers indicates an additional level of complexity and cellular specialization. While PT is also characterized by multiple contributors and can be considered multi-cellular the cellular specialization found at UD is lacking and suggests that predation (selection) is much stronger on that population and recent events such as the Kitzmiller decision support that conclusion. The resultant population stability observed in newly evolved multi-cellular Chlorella algae suggests that ID and belief based notions about biological complexity will continue to survive. Since it is hypothesized that minimum cluster size is dependent upon nutrient access, the best method to combat large clusters is better science education reducing available nutrients.

Delta Pi Gamma (Scientia et Fermentum)

Comment #79614

Posted by BlastfromthePast on February 14, 2006 12:10 AM (e)

It seems quite obvious that there was simply an environmental response on the part of Chlorella when in the presence of a predator. It’s much harder to “eat” a multicellular globule. It’s quite obvious that the “machinery” for responding is “built-in”. This isn’t evolution in the least.

This highlights the difference between ID and neo-Darwinism: experiments like this are completely misunderstood.

Comment #79616

Posted by Sir_Toejam on February 14, 2006 12:23 AM (e)

This highlights the difference between ID and neo-Darwinism: experiments like this are completely misunderstood

lol. that’s just perfect, blasty.

couldn’t have said it better myself. Now if you could only realize the truth of what you said is the exact opposite of the meaning you intended.

*sigh*

Comment #79617

Posted by PvM on February 14, 2006 12:25 AM (e)

Blast wrote:

It seems quite obvious that there was simply an environmental response on the part of Chlorella when in the presence of a predator. It’s much harder to “eat” a multicellular globule. It’s quite obvious that the “machinery” for responding is “built-in”. This isn’t evolution in the least.

This highlights the difference between ID and neo-Darwinism: experiments like this are completely misunderstood.

ROTFL, but no it was not an induced response and the researcher tested against such scenario but rather more likely a rare mutation being selected for. There are many good reasons why your ‘explanation’ fails. If it were a built in response, why did it take 100 generations and many dead ‘algae’ before slowly multicellular forms arose?

Under non-predation circumstances, the cost of colonization may be too high but add in another factor and voila speciation, and not just any speciation but an important step from single to multicellular.

So why is it not evolution:
1. Variation
2. Selection
3. Speciation

As to your ‘explanation’ could you be more specific as to the details? What machinery, when was it ‘built in’? You know, them pesky, what did Dembski again call them? oh yes, pathetic details.

Given the response, is there anyone left who denies that ID is scientifically vacuous?

Comment #79618

Posted by Pvm on February 14, 2006 12:28 AM (e)

Sir Toejam, that’s funny, had not noticed the Freudian slip here. Why is it so hard for ID activists to accept evolutionary theory? I thought that ID embraced evolutionary theory? After all, that’s why it presents no real scientific explanations of its own relevant to its thesis.

Comment #79621

Posted by PvM on February 14, 2006 12:34 AM (e)

If Blast is interested in examples of induced response, then there are good papers out there

Hessen and Van Donk (1993) discovered the involvement of a chemical cue released from the zooplankton in stimulation of colonies. The addition of filtered medium from a Daphnia culture to unicellular Desmodesmus subspicatus populations resulted within two days in populations dominated by colonies, while the controls remained unicellular.

Comment #79622

Posted by Sir_Toejam on February 14, 2006 12:37 AM (e)

as to why it is apparently so hard to get IDers to recognize the science involved in evolutionary theory, and the tremendous evidence in support, I came to the conclusion long ago that most are suffering from a common psychological disorder.

go take a look at a freshman psych text that goes into standard freudian defense mechanisms sometime.

the physchological pressure these folks feel between their constructed belief systems and the reality of the world as it presents itself to them motivates them subsconsciously to produce ever more extreme and bizarre forms of defense mechanisms.

typically, these seem to take the form of projections, as blast has just so wonderfully demonstrated for us just now, and frequently has in the past.

Denial is also a very common defense mechanism among many ID supporters.

I swear, someone could easily write a series of papers extolling the remaining virtue in freudian psychology simply by using creationists as a research group.

Comment #79623

Posted by PvM on February 14, 2006 12:41 AM (e)

As I explained Boraas et al also discussed the induction alternative and rejected it based on the following reasons

Our results could be interpreted as evidence that the flagellates released a substance inducing colony formation in Chlorella, similar to predator-induced morphological changes in zooplankton (Dodson, 1989) and in coccoid green algae (Hesssen and van Donk, 1993). We discount this alternative hypothesis, based on four observations. First, colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates. An ‘induction’ should have been expressed as soon as the inducing substance produced by the flagellates had reached some critical concentration. Secondly, once it has appeared, the colonial growth form has been maintained in mixed-species cultures for over 2 years, even at low flagellate densities. Induction should vary with flagellate density. Thirdly, when the colonies are cultured in the absence of any source of an inducing substance, the colonies ‘breed true’. The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have beenmaintained for several months. Finally, in nitrogen-limited, two-stage chemostats where both stages are illuminated, with unispecific Chlorella in the ®rst stage and mixed Chlorella-Ochromonas in the second stage, we see colonial Chlorella. These Chlorella must be growing on the inorganic nitrogen excreted by Ochromonas. When the second stage is darkened, the Chlorella colonies rapidly wash out of the culture, leaving only the unicellular Chlorella supplied from the first stage and, of course, their flagellate predators. This shows that active photosynthesis by the algae and continued interaction with the predator are essential to maintain the colonial algae in continuous culture. When cultured in the absence of the predator, the cell size of the unicells in the second stage declines, showing that cell division and associated morphogenetic processes are taking place, but the colonies are not formed in the absence of the predator.

Hope this helps. Don’t worry, there is far more fascinating stuff. Multicellularity, evolution of sex… Cool stuff.

Comment #79625

Posted by PvM on February 14, 2006 1:12 AM (e)

Wikipedia has some interesting stuff on cognitive dissonance see also here

Our minds work in mysterious ways and such little time to learn about all this cool stuff.

Comment #79630

Posted by Sir_Toejam on February 14, 2006 1:57 AM (e)

yes, I’ve heard the conflict between some religious worldviews and objective reality described as a form of congnitive dissonance before; more specifically, the wiki article you mentioned best describes this as follows:

The more well-known form of dissonance, however, is post-decisional dissonance. Many studies have shown that people with compulsive disorders like gambling will subjectively reinforce decisions or commitments they have already made. In one simple experiment, experimenters found that bettors at a horse track believed bets were more likely to succeed immediately after being placed. According to the hypothesis, the possibility of being wrong is dissonance-arousing, so people will change their perceptions to make their decisions seem better.

it sounds ludicrous to those who aren’t suffering from this that someone would actually “change their perceptions to make their decisions seem better”, but it’s been documented so many times as to be considered commonplace.

now, I’m not saying that all of ID exists solely becuase of some psychological schism. Indeed, there is a lot of evidence to indicate that the specifics of the strategy may have been designed as more political strategy (not for ideology’s sake, but merely to better control and maintain a significant grassroots power base) than as a result of ideological postulates.

However, from what I have seen of many creationists (blast being a great example), the tenants of ID seem almost tailor-made to act as a lure for those suffering from the type of dissonance I am speaking of here, just as “creation science” was 40 years ago.

this would also explain why a large proportion of xians in the US (and around the world) are NOT attracted to ID. they simply aren’t suffering this type of dissonance.

Along with politicians, who are using ID in order to maintain their right-wing political base (think Santorum and GW as good public examples), the other “pushers” taking advantage of this are those doing it to make money, like Dembski. This explains why folks like Dembski, who are obviously more intelligent than they “play on TV”, keep repeating the same drivel over and over again, even though they themselves admit to the inadequacy of ID as science, or even theory. They know they have a “captive audience”, desperate to have someone throw out something to alleviate their dissonance; something they can easily “change their perceptions” to fit their worldview.

It’s very much like a pusher selling crack to the addicted.

It’s not the motivations of folks subject to a psychological disorder, like blast, that disgust me. It’s the pushers like Dembski, and the “casino owners” like GW.

True conservative republicans have been deriding the reliance on this powerbase for decades now.

However, instead of a decreasing placation and manipulation of this group, the current neocons, led by Karl Rove, instead seem to be expanding their abuse of these folks in order to gain ever more power and control.

It sickens me to no end.

Comment #79695

Posted by BlastfromthePast on February 14, 2006 9:27 AM (e)

PvM wrote:

ROTFL, but no it was not an induced response and the researcher tested against such scenario but rather more likely a rare mutation being selected for. There are many good reasons why your ‘explanation’ fails. If it were a built in response, why did it take 100 generations and many dead ‘algae’ before slowly multicellular forms arose?

You say that it’s “more likely a rare mutation”. So you don’t know. You’re guessing.

Now, if it’s a “rare mutation”, a “rare mutation” in what? ONE of the chlorella? Or is it a case of “simultaneous rare mutations” in a number of the chlorella?

Multicellularity is a kind of “social” behavior on the part of the chlorella, so perhaps that’s why it takes time (100 generations) to bring about. It’s entirely possible that the chlorella start producing some kind of protein in the presence of predators which, when reaching a certain critical concentration, triggers the multicellularity response.

You say it’s not an “induced” response. But, of course, it is one way or the other: viz., whether it is ‘induced’ by the ‘predator’ or induced by some other chemical/protein, it’s an ‘induced’ response.

And how did the experimenter test that this wasn’t the case? It would have been nice to have included that information.

Comment #79719

Posted by AD on February 14, 2006 10:41 AM (e)

You say that it’s “more likely a rare mutation”. So you don’t know. You’re guessing.

Now, if it’s a “rare mutation”, a “rare mutation” in what? ONE of the chlorella? Or is it a case of “simultaneous rare mutations” in a number of the chlorella?

Multicellularity is a kind of “social” behavior on the part of the chlorella, so perhaps that’s why it takes time (100 generations) to bring about. It’s entirely possible that the chlorella start producing some kind of protein in the presence of predators which, when reaching a certain critical concentration, triggers the multicellularity response.

You say it’s not an “induced” response. But, of course, it is one way or the other: viz., whether it is ‘induced’ by the ‘predator’ or induced by some other chemical/protein, it’s an ‘induced’ response.

And how did the experimenter test that this wasn’t the case? It would have been nice to have included that information.

Allow me to address some of this in pieces:

1) “Most likely” is not referring to an uneducated guess here. This is an educated conjecture based on data that is sufficient to establish a degree of certainty, but not 100% truth in all situations bar none no matter what. He’s not just “guessing”. You misconstrue the wording, and I think it’s probably deliberate, as the other option is that you’re quite plainly not very bright.

2) Mutations occur in DNA sequences. I’m not really sure what your question is, but it appears nonsensical to me. I have not read the study, obviously, but the implication seems to be that a mutation occurred in a single-celled organism which encouraged it to either itself become multi-cellular OR allowed it to, in some way, gather other single-celled organisms into a larger whole. I’d have to research it to give you a good answer… but you could answer your question yourself by researching it. Again, I think it is willful ignorance that prevents this. If you legitimately don’t know how to research, I’m sure if you ask politely we’d be happy to share.

3) As to your third paragraph - I see a 20 generation timeframe for the initial multi-cells to erupt onto the scene, and then over time (should they have an advantage in reproduction thanks to survivability, which they did) they would gradually become the dominant force. This is what occurred. Precisely what is your question getting at? As to the “producing a protein” part, again, read the summary alone. They address that, and if that was true, you would not need the many generations that passed in order to undergo a change. I’m also pretty sure you could control and/or test for it. If you think that’s the correct theory, I suggest you actually test it! They have produced results - if you dispute them, you must do the work to disprove them yourself. The burden of proof is now on you.

4) You are not using the same definition of induced as the author of this summary, and that is where your confusion comes from here. In their case, “induced” is not meant to include the natural environmental pressure from the predators. In your case, it is. Sort that out and you see the problem. Again, I think you are doing this willfully, or are you incapable of basic reading comprehension?

So, in closing, I see some problems. You change contexts wildly and then try to argue the original arguments based on an entirely different context. You are using different definitions from the authors, but attempt to superimpose your definitions on theirs and thus alter the message they were conveying improperly. Lastly, you display (willful?) ignorance of the scientific process in very basic and fundamental ways. I suggest you learn how to rectify these issues in the future, lest you be taken even less seriously than you currently are. I’m not saying this to be a jerk, either - I fully welcome informed debate by all sides.

I tire, however, of wildly uninformed “debate” (and I use that word only in the most sarcastic sense possible).

Comment #79769

Posted by Jason on February 14, 2006 12:55 PM (e)

Test it yourself! That’s too much. I’m sorry.

And btw, of course, I think ID is a waste of time and can explain nothing, but please…

Comment #79854

Posted by Sir_Toejam on February 14, 2006 3:39 PM (e)

Multicellularity is a kind of “social” behavior on the part of the chlorella, so perhaps that’s why it takes time (100 generations) to bring about. It’s entirely possible that the chlorella start producing some kind of protein in the presence of predators which, when reaching a certain critical concentration, triggers the multicellularity response.

changing perceptions to fit worldview.

check.

It’s not even CLOSE to being in the same category as any kind of correctly defined social behavior Blast.

Can’t you see how you are twisting your own perceptions?

hell, you’re going so far as to try to put square pegs into round holes even!

Comment #79856

Posted by BlastfromthePast on February 14, 2006 3:42 PM (e)

AD wrote:

I’m not saying this to be a jerk, either - I fully welcome informed debate by all sides.

That’s quite nice of you. May I point out a few things:

(1) When it came to responding to what I said was no more than a ‘guess’, you respond that it is an “educated guess”. How very informative!
(2) When I ask if the ‘mutation’ is in ONE of the chlorella or more than one you respond by saying “the implication seems to be that a mutation occurred in a single-celled organism which encouraged it to either itself become multi-cellular OR allowed it to, in some way, gather other single-celled organisms into a larger whole. I’d have to research it to give you a good answer.” You’re guessing. Is that “informed debate”?
(3) Regarding the ‘multicellularity’ you seem to suggest that they covered that (And I presumed that they TRIED to cover that.). But without knowing further details, it’s hard to know. You yourself write: “They address that, and if that was true, you would not need the many generations that passed in order to undergo a change. If that were true? Is this informed debate too?
(4)As to “inducing”, you write: You are not using the same definition of induced as the author of this summary, and that is where your confusion comes from here. In their case, “induced” is not meant to include the natural environmental pressure from the predators. Why do you assume I’m “confused”? You write that “in their case ‘induced’ is not meant to include the natural environmental pressure from the predators. Thank you for pointing out the obvious. The point is that ‘induced’ has a generalized meaning; and within that generalized meaning, the presence of the predator brings about a response (induced) in Chlorella. Did you notice my last comment where I said that it would have been nice for them to have included this information. Again, let’s hear it for “informed debate”. I’m waiting for the information.

Comment #79857

Posted by BlastfromthePast on February 14, 2006 3:45 PM (e)

Sir Toe Jam wrote:

hell, you’re going so far as to try to put square pegs into round holes even!

Yeah, and when you put quotation marks around a word, it’s possible to fit square pegs into round holes. Or are you not paying attention?

Comment #79861

Posted by Sir_Toejam on February 14, 2006 3:56 PM (e)

putting quotes around a word does not totally change its meaning, except maybe in your own mind there, blasty.

it implies the word generally fits the category of usage, with exceptions.

however, in the way you use it, you might as well have used the word “metallic”.

you selective use of quotes around words only serves to indicate the spots where you are selectively applying your very own constructed perceptions.

hence that’s why i made a point of it.

you exhibit this behavior commonly. perhaps without even realizing it. You ARE suffering from a form of dissonance.

As to whether that’s curable or not, you’d have to visit a mental health professional.

no shame in that; mental illness is just like any other physical ailment.

I wish you luck.

Comment #79873

Posted by AD on February 14, 2006 4:24 PM (e)

Blasty,

Let’s try this again, but if you continue to use the same disingenuous tactics, I’m going to cease bothering:

1) You disparagingly called something a guess, with the implication being that it was obviously unfounded. An educated guess (also known as a professional estimation) is something that is well-founded but accepts a small degree of potential uncertainty. These are not the same thing. For instance, you would be guessing what color my dog is, but I could make an educated guess about the potential standard deviation on a specific set of data, given that I’m a mathematician.

2) A mutation, by definition, is contained within one strand of DNA. This is why your question is nonsensical. Concurrent identical mutation across multiple organisms is something that is not predicted (unless there is some method of directly transferring DNA between non-offspring relational organisms) by evolution, thus IF that is what you were asking, your question is just plain stupid. It should be obvious that’s not the case, if you had done the background research. My “guess”, which is in this case an “educated guess”, as above, is predicated around that fact which you were apparently not in possession of. Also, you might notice I advised you to verify, which you shockingly failed to do. I made an educated guess and informed you how to check it, yet you both failed to understand that and then failed to check it.

3) You’re cherry picking my quotes here. Let’s back up and add that magical thing known as context. First, there are statements about your comment on the cause of multi-cell colonies in the summary of the article. So let me ask you: did you not read it, or did you not understand what you read? We’re out of other options, because you just claimed they didn’t address it. Which one was it? Secondly, when I said “IF that were true” I was alluding to your previous statement, with the implication being that it was not, in fact, true. In the same way I now say that if you were capable of even a basic level of reading comprehension, we wouldn’t be having this discussion, because you’d already have realized your questions were answered. However, that’s obviously not the case. I assumed (foolishly) that you were not so stone cold stupid as to be incapable of picking up on very basic and commonly used implication in the english language. I was quite clearly wrong.

4)

Thank you for pointing out the obvious. The point is that ‘induced’ has a generalized meaning; and within that generalized meaning, the presence of the predator brings about a response (induced) in Chlorella.

Except that they weren’t using the generalized meaning! This is precisely the problem you are having. I can certainly claim that “engine” has a generalized meaning that might refer to say, a steam or coal engine, but it’s understood that when an auto mechanic speaks about a car engine, he’s referring to an internal combustion engine. Well, that is, unless you’re too dense to pick up on context, which again appears to be the case here. They weren’t using the generalized meaning. If you try to apply a generalized meaning to their argument in response, you’re just plain wrong.

Thus, if you’re going to post again, I suggest that you either become literate in a most basic fashion and learn how to fact-check, or that you actually stop being a lying, disingenuous snake, depending on which is the case. Also, I notice you still have not offered to perform any experiments or back up your conclusions, when the burden of proof is upon you. You fail on multiple levels here, and I think that should be apparent to the general audience reading this thread. Should you continue to replicate these failures (or introduce similarly obvious ones), I’ll stop wasting time on you.

Better luck with your next post.

Comment #79917

Posted by BlastfromthePast on February 14, 2006 5:59 PM (e)

Dear AD:

Bile does not substitue for erudition. So try a different tact, please.

(1)“You disparagingly called something a guess, with the implication being that it was obviously unfounded.” Just because you don’t like it doesn’t make it anything different than a “guess”. So what if it’s an educated guess. Isn’t science supposed to move us beyond guesses? And it’s only an “educated” guess if you believe that RM+NS actually does miraculous things. I don’t happen to believe that. And you don’t have “proof” of that: you have “educated guesses”. That’s not sufficient. Sorry.
(2)“A mutation, by definition, is contained within one strand of DNA. This is why your question is nonsensical.” Am I to understand that just because some scientist says “evolution did it”, that I am to assume that a mutation occurred, and that that mutation brought about the observed change? Where is the mutation? What was the sequence change? What does it look like? Or am I simply to take it on “faith” that somewhere, somehow, a cytosine molecule changed to a glycosine, and voila–multicellularity. I’m simply not that gullible. Again, sorry.
(3) “Secondly, when I said “IF that were true” I was alluding to your previous statement, with the implication being that it was not, in fact, true.” I apologize. I did misread what you wrote. Part of the reason for that is that the reasoning that Borass uses is a little bit far-fetched; viz., just because a response didn’t happen quickly, it’s not induction? he scratches his head> What rule says that induction has to act quickly? In fact, to turn the tables on him, there’s every good reason to expect “induction” not to take place quickly if, in fact, the ‘colony’ form persists for two years as he states. If it’s so hard for the organism to go back to the unicellular form, then it might have a very high, complex, threshold for “switching” over to the multicullular form.
(4) “They weren’t using the generalized meaning. If you try to apply a generalized meaning to their argument in response, you’re just plain wrong.” Now let me see. They say that in order for the “colonies” to persist, the predator has to be present. And when the predator is taken away then the colonies go away. Is there not enough room in the word “induction” to cover such a situation? The only reason that they don’t use “induction” is because it took 20 generations to bring about an initial change. To them that’s “proof” that “induction” didn’t take place. Again, where’s the rule that says that “induction” has to take place quickly?

(5)“Also, I notice you still have not offered to perform any experiments or back up your conclusions, when the burden of proof is upon you.”

Tell me: what have they “proved”? Have they proved it was an “mutation”? No: it’s an “educated” guess. Have they proved that some process of “induction” is involved? No, they simply infer that “induction” ought to occur more quickly. It’s not me that needs to “prove” something; it’s them. They’re simply postulating a mechanism–i.e., hand-waving. Sorry, I’m not that gullible.

Here is this great irony: the neo-Darwinists claim that science will come to a halt if IDers take over (they’re creationists, after all), and what we end up seeing is neo-Darwinists coming to a standstill in the laboratory because RM+NS says the problem’s solved. Well, it isn’t solved. There are a lot more questions to be pursued.

And I stand by my initial assessment: this phenomena is, plain and simple, an induced reaction by the chlorella in response to an environmental stimulus. Prove me wrong!

As I said above: isn’t science supposed to move us beyond guesses?

Comment #79919

Posted by BlastfromthePast on February 14, 2006 6:03 PM (e)

Sir Toe Jam wrote:

As to whether that’s curable or not, you’d have to visit a mental health professional.

no shame in that; mental illness is just like any other physical ailment.

So, it seems that the high priests of Darwinism have moved beyond the Inquistion and “witch trials”, and are now employing that tactics of Stalinist Russia to stamp out dissent.
“He doesn’t believe in Communism. He must be mentally ill.”

Tell me: are you guys religious fanatics, communist dictators, or just plain fascists? I’m curious to know.

Comment #79924

Posted by PvM on February 14, 2006 6:10 PM (e)

Ah, the sound of denial… A first step towards recovery from cognitive dissonance

Comment #79925

Posted by PvM on February 14, 2006 6:13 PM (e)

Blast wrote:

They say that in order for the “colonies” to persist, the predator has to be present. And when the predator is taken away then the colonies go away. Is there not enough room in the word “induction” to cover such a situation? The only reason that they don’t use “induction” is because it took 20 generations to bring about an initial change. To them that’s “proof” that “induction” didn’t take place. Again, where’s the rule that says that “induction” has to take place quickly?

Nope, they gave four reasons. Have you not been following the discussion? Or have you not read the paper (eeks!!!)

Comment #79926

Posted by PvM on February 14, 2006 6:17 PM (e)

There is nothing miraculous about this experiment. The algae have a rare variant which is multicellular. When under environmental pressure, such variants are ‘amplified’ leading to colonies of 4 to hundreds of cells, finally reaching a steady state of 8.

Thirdly, when the colonies are cultured in the absence of any source of an inducing substance, the colonies ‘breed true’.

Why so much opposition to what science has found? If Blast disagrees, he can present his own research and experiments to support his claims. But induction was considered and rejected on good grounds.

Comment #79929

Posted by PvM on February 14, 2006 6:19 PM (e)

And it either way the response is induced then why are we arguing? You seem to be suggesting that your induction idea is similar to the selection argument?

Comment #79945

Posted by BlastfromthePast on February 14, 2006 7:05 PM (e)

PvM: You’re always even-headed and open-minded. Good for you.

You wrote, in relation to the possibility of “induction”: “Nope, they gave four reasons. Have you not been following the discussion?”

Well, here’s the problem:

Thirdly, when the colonies are cultured in the absence of any source of an inducing substance, the colonies ‘breed true’. The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have beenmaintained for several months…. (later on)This shows that active photosynthesis by the algae and continued interaction with the predator are essential to maintain the colonial algae in continuous culture.

This doesn’t seem to rule out the possibility of the predator flagellate being the “inducer”: meaning that it interacts with chlorella, either directly or indirectly, bringing about a pre-packaged response in the Chlorella.

Is there some technical detail I’m missing here?

Comment #79958

Posted by 'Rev Dr' Lenny Flank on February 14, 2006 7:37 PM (e)

Bile does not substitue for erudition. So try a different tact, please.

Erudite us, Blast. Explain to us how “frontloading” works.

(sound of crickets chirping)

Yep, that’s what I thought. All mouth.

Comment #79969

Posted by Jason on February 14, 2006 7:58 PM (e)

I read through the whole paper and I guess I can’t see where they say that there is evidence for any mutation that took place within those first 10 days of Chlorella recovery where the first colonies were observed.

Discussion section wrote:

We discount this alternative hypothesis, based on four observations. First, colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates.

They emphasize the 10-20 generations part, but de-emphasize when the colonies first appeared, which was during the very first rebound of the Chlorella population.

Results section wrote:

This reduction in predation pressure allowed the Chlorella population to recover and increase rapidly, in the manner of a classical predator-prey oscillation. During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a). The number of cells per colony ranged from four to hundreds (Fig. 1c), bracketing and masking the flagellate size distribution (Fig. 2a).

The colonies were observed on the very first population rebound.
Then later in the paper, they allude to the fact that the Chlorella revert to their unicellular form when the predator isn’t there.

If they introduce the predator again, they see the same sort of colonies in exactly the same way, don’t they?

This looks like a microscopic version of peppered moths and nothing more.

I highly doubt that there was any kind of mutation that took place within that rebound period that is responsible for colony formation.

Something tells me that if you found some similar unicellular Chlorella in the wild, cultured it for only a few generations (not 3 decades), and introduced a phago-predator, you’d see the reversible colony formation.

I understand why the authors use this mechanism to hypothesize that multicellularity arose because of predator-prey relationships in the pre-Cambrian and it is reasonable. I just don’t see why they believe that a favorable mutation occured within the first rebound period within this particular experiment.

Someone please tell me where I’m wrong.

Comment #79970

Posted by Jason on February 14, 2006 8:00 PM (e)

Nope, nevermind.

I see it now. This has already been covered.

PvM wrote:

The algae have a rare variant which is multicellular. When under environmental pressure, such variants are ‘amplified’ leading to colonies of 4 to hundreds of cells, finally reaching a steady state of 8.

Got it.

The paper is unclear about this.

Comment #80012

Posted by Sir_Toejam on February 14, 2006 10:37 PM (e)

Tell me: are you guys religious fanatics, communist dictators, or just plain fascists? I’m curious to know.

hmm. If i have to pick, I’ll go with communist dictator; provided i get to pick the form of communism.

could be fun.

Comment #80015

Posted by PvM on February 14, 2006 11:25 PM (e)

Thirdly, when the colonies are cultured in the absence of any source of an inducing substance, the colonies ‘breed true’. The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have beenmaintained for several months…. (later on)This shows that active photosynthesis by the algae and continued interaction with the predator are essential to maintain the colonial algae in continuous culture.

This doesn’t seem to rule out the possibility of the predator flagellate being the “inducer”: meaning that it interacts with chlorella, either directly or indirectly, bringing about a pre-packaged response in the Chlorella.

So colonies are induced and then maintain themselves and ‘breed true’ over long periods of time. As far as the continuous culture is concerned you have to understand how the chemostats work. There is a first chamber where chlorella algae are being grown for the predator in the second chamber. When the light in the second chamber is turned off, the multicellular algae do not survive and only unicellular ones from the first chamber remain to replenish the second chamber.

The evidence strongly suggests against a inducer as you seem to have in mind.

Jason wrote:

If they introduce the predator again, they see the same sort of colonies in exactly the same way, don’t they?

This looks like a microscopic version of peppered moths and nothing more.

Most of the times the colonies return in repeat experiments. I believe the paper mentions in about 70% of the time. It’s a version of the peppered moth, only with a major difference the new species are in a completely new family.

It seems that some confuse Darwinian theory with mutations arising when needed. Rather a better example is that Darwinian theory relies on existing variation and when selective pressures change, organisms with a mutation can spread quickly and replace the original organisms. In this case the difference between the two organisms caused the two version to be in two separate families.

Details in the paper suggest that incomplete cell division may have ‘caused’ the cells to ‘stick together’ and be surrounded by a membrane. Selective pressures were a balance between efficiency (few cells the more efficient) and predator evasion (more cells the safer).

If the switch from single to multicellular is argued to be nothing more than micro evolution then it seems that there may be really no limits to microevolution after all.

Comment #80018

Posted by PvM on February 14, 2006 11:41 PM (e)

A later paper gives the following helpful comments

Whereas some predators secrete pheromones that can induce colony formation in their prey, the transition to multicellularity in this example was heritable and stable in the absence of the predator. The rapid evolution of multicellularity demonstrates a latent and normally untapped genetic potential within populations of C. vulgaris. Furthermore, it lends credence to the idea that predation may have selected for fixation of multicellularity in the unicellular progenitors of animals.

Nicole King, The Unicellular Ancestry of Animal Development, Developmental Cell, Vol. 7, 313–325, September, 2004,

Also there is a 5th reason why induction does not seem to be a very good thesis. In only 70% of the replicants did the experimenters see a repeat of multicellularity. This is understandable from a selection perspective but not from an induction perspective.

Also notice the ‘stable in absence of predator’…

Comment #80095

Posted by AD on February 15, 2006 10:34 AM (e)

PvM, you are more patient than I.

I think, however, Blast’s comments have made the case against him far better than anything else I could continue to say in this thread, so I’m done here. Either way, I firmly believe an unbiased reader would very quickly be able to determine which side was playing fair and presenting rational arguments, and which side was not.

Enjoy.

Comment #80098

Posted by Rilke's Granddaughter on February 15, 2006 10:41 AM (e)

Squib from the Past wrote:

Tell me: are you guys religious fanatics, communist dictators, or just plain fascists? I’m curious to know.

I’m an unrepentant monarchist, actually. After all, genetics occasionally throws up competence; popularity contests guarantee you don’t get it.

Comment #80102

Posted by ben on February 15, 2006 10:57 AM (e)

The evidence strongly suggests against a inducer as you seem to have in mind.

Don’t worry, the “inducer” will stay in his mind regardless of what arguments or evidence are offered.

Comment #80106

Posted by William E Emba on February 15, 2006 11:18 AM (e)

BlastfromthePast wrote:

Tell me: are you guys religious fanatics, communist dictators, or just plain fascists? I’m curious to know.

I can’t speak for the rest, but yes, I am a religious fanatic, of the right-wing observant Judaism variety. As such, I am absolutely opposed to my taxes being used to engage in any form of religious indoctrination in the schools. The Church of Designtology can huckster in partnership with the Campus Crusade for Christ all they want–just not on my dime.

Comment #80159

Posted by BWE on February 15, 2006 3:03 PM (e)

Posted by Jason on February 14, 2006 12:55 PM (e)

Test it yourself! That’s too much. I’m sorry.

And btw, of course, I think ID is a waste of time and can explain nothing, but please…

No Jason, it is not too much. Assuming we are peers :P reviewing this work as Blast is attempting to do, we need to point out flaws in the design of the experiment. So Blast says:

Now let me see. They say that in order for the “colonies” to persist, the predator has to be present. And when the predator is taken away then the colonies go away. Is there not enough room in the word “induction” to cover such a situation? The only reason that they don’t use “induction” is because it took 20 generations to bring about an initial change. To them that’s “proof” that “induction” didn’t take place. Again, where’s the rule that says that “induction” has to take place quickly?

as an attempt to point out a flaw in the design of the experiment.

So as the team of peer reviewers, we should examine his point and determine if the experiment needs more refinement to be able to judge the results as valid. If we were in agreement that this science is faulty, I could design an experiment to demonstrate this. Usually by tweeking one or two elements of the original experiment at a time.

So, “test it yourself” is Precicely the right thing to say. We can point out the potential flaws in the design of the experiment, but unless they are known flaws with known ability to skew results, we would then need to design an experiment to prove that the first experiment was faulty.

That is actually waaaaay shorthand for the point I am trying to make here but I am remembering back to a time when I used another guy’s data in my thesis work and my prof made me do the whole friggin thing over with new numbers and I had to get the data myself because the context was different. Took me nearly 3 months to make the changes. 20 years later I’m still pissed because I got exactly the same data.

Blast, for example, is my prof saying, “this is nonsense because they didn’t limit for induction well enough.”

AD Wrote
3) As to your third paragraph - I see a 20 generation timeframe for the initial multi-cells to erupt onto the scene, and then over time (should they have an advantage in reproduction thanks to survivability, which they did) they would gradually become the dominant force. This is what occurred. Precisely what is your question getting at? As to the “producing a protein” part, again, read the summary alone. They address that, and if that was true, you would not need the many generations that passed in order to undergo a change. I’m also pretty sure you could control and/or test for it. If you think that’s the correct theory, I suggest you actually test it! They have produced results - if you dispute them, you must do the work to disprove them yourself. The burden of proof is now on you.

Aarg, I have to go. I’ll be back to finish this post.

Comment #80171

Posted by pondscum on February 15, 2006 3:51 PM (e)

As an addendum to the discussion of NS in Chlorella, algal biologists, particularly those that cultivate unialgal and axenic lines, have been aware that changes do occur. A quick survey of the UTEX culture collection identifies several strains that have lost the ability to reproduce sexually or to form stages typical of the original isolate. Of course, asexual reproduction continues to work like a charm. While the loss of sexuality is an annoying issue for researchers interested in studying sexual reproduction in these cultivated lines, it offers strong support to the notion that mutation and selection have been at work. One might ask why these putative mutations haven’t been identified. Well, largely because its costs big $$$ to do a genome. The Chlamydomonas reinhardtii genome is just now being annotated—this would have to be our starting point, but we still know so little about any algal genome. So many mutations, so little time and money.

Comment #80257

Posted by Jason on February 15, 2006 8:57 PM (e)

PvM wrote:

Most of the times the colonies return in repeat experiments. I believe the paper mentions in about 70% of the time. It’s a version of the peppered moth, only with a major difference the new species are in a completely new family.

New species? Different family?

You said so yourself that it’s a variant of the same species.

Are you suggesting that there are two types of organisms from different families living in the same colony?

Here’s a “test it yourself” situation then. We could try to pipette out one or a few unicellular forms, and make sure we have absolutely no colony forms in the mix. Culture those until there are plenty enough to repeat the experiments in the paper. Then, I’d bet you dollars to donuts that you’d see colony formation. I’d bet that the ability to form colonies is just part of the genome. It’s ONE species.

In this case the difference between the two organisms caused the two version to be in two separate families.

Maybe by arbitrary assignment they were in different families.

If the switch from single to multicellular is argued to be nothing more than micro evolution then it seems that there may be really no limits to microevolution after all.

To me, the micro/macro evolution dichotomy is a false one.

No Jason, it is not too much. Assuming we are peers :P reviewing this work as Blast is attempting to do, we need to point out flaws in the design of the experiment.

Test it yourself is a silly thing to say on an internet comment board.

Obviously, unless blastfromthepast is a microbiologist, he won’t have the resources to test it himself.

I think any person may critique or criticize a paper all they want, especially on the internet, but they don’t have to be in that
particular field to have a point. And they certainly don’t have to prove it to you by the huge task of writing a proposal, getting funded, doing the research and publishing it, all to make a point on an internet comment board.

That’s why I said that it’s too much.

Comment #80258

Posted by Jason on February 15, 2006 8:59 PM (e)

Colony above should read “culture.”

Comment #80261

Posted by Sir_Toejam on February 15, 2006 9:17 PM (e)

I think any person may critique or criticize a paper all they want, especially on the internet, but they don’t have to be in that
particular field to have a point. And they certainly don’t have to prove it to you by the huge task of writing a proposal, getting funded, doing the research and publishing it, all to make a point on an internet comment board.

i suppose that depends entirely on how valid you wish your point to be, and what that point intends to address.

If you want to address the grammar of the paper, you certainly don’t have to even be an english major, but if you want to critique the methods or conclusions of a scientific paper, your point is better made if you have studied the subject material, and understand at least how experiments in the subject matter at hand are designed.

saying to someone “test it yourself” is a slap at the fact that the persona it was directed at in fact has NO clue at all about algal physiology, ecology, or even how one goes about beginning to answer questions about same.

so what’s your point then?

that there are errors in the paper, or that internet commentary in general isn’t worth the time taken to type it?

Comment #80267

Posted by Henry J on February 15, 2006 10:21 PM (e)

IOW, those mean scientists just ruined the sex lives of those poor critters… ;)

Henry

Comment #80272

Posted by Anton Mates on February 15, 2006 11:27 PM (e)

Jason wrote:

New species? Different family?

You said so yourself that it’s a variant of the same species.

Are you suggesting that there are two types of organisms from different families living in the same colony?

Here’s a “test it yourself” situation then. We could try to pipette out one or a few unicellular forms, and make sure we have absolutely no colony forms in the mix. Culture those until there are plenty enough to repeat the experiments in the paper. Then, I’d bet you dollars to donuts that you’d see colony formation. I’d bet that the ability to form colonies is just part of the genome. It’s ONE species.

I think the “different family” thing Pim’s talking about is taken from talk.origins, and I believe it’s in error…the family they suggested the multicellular morph keys out in (Coelosphaerium) is prokaryotic, which is almost impossible to believe. I’m gonna try to hunt down one of their references tomorrow, see if they misread it.

That said, I believe the multicellular morph would key out as a different species. Not only is it single-celled versus multicellular–a huge morphological difference in itself–but they observed other related differences between the two in terms of reliance on photosynthesis, success in low-nutrient environments and (obviously) resistance to predation. I’m no expert on defining species in asexual organisms, but I know they’ve been defined on much less than that.

While it’s true that you apparently see colony formation pretty reliably when you repeat the experiment, that doesn’t mean “the ability to form colonies is just part of the genome.” It means that the genome can reliably be modified by mutation to gain that ability. And in turn that doesn’t mean that the genome is somehow set up to produce one particular mutation. You’ll notice that the actual genetic mechanism for colony formation must have differed somewhat between colonies, because there were a ton of different colony sizes at first before the eight-cell colonies won out. That suggests that lots of different mutations are possible which all result in various multicellular morphs.

The researchers just hit upon a study organism and a selection pressure which was remarkably well-suited to induce speciation. What I’d love to see is if they could set up an environment which had stable populations of the morphs living side by side…maybe a chemostat with the flagellate predator and an illumination gradient?

To me, the micro/macro evolution dichotomy is a false one.

I think most evolutionary biologists would agree, and experiments like this support that view.

Henry J wrote:

IOW, those mean scientists just ruined the sex lives of those poor critters… ;)

Actually, I think Chlorella’s obligately asexual, so normally it just has to do it all by itself…at least now the cells get to reproduce in company!

Comment #80275

Posted by Henry J on February 15, 2006 11:50 PM (e)

Anton,
Actually, my “those mean scientists just ruined the sex lives of those poor critters”
was referring to pondscum #80171 “A quick survey of the UTEX culture collection identifies several strains that have lost the ability to reproduce sexually or to form stages typical of the original isolate”
rather than the Chlorella.

Henry

Comment #80277

Posted by Anton Mates on February 16, 2006 12:18 AM (e)

Henry J wrote:

Anton,
Actually, my “those mean scientists just ruined the sex lives of those poor critters”
was referring to pondscum #80171 “A quick survey of the UTEX culture collection identifies several strains that have lost the ability to reproduce sexually or to form stages typical of the original isolate”
rather than the Chlorella.

O! Mea culpa.

Bastards!

Comment #80279

Posted by PvM on February 16, 2006 12:22 AM (e)

I think the “different family” thing Pim’s talking about is taken from talk.origins, and I believe it’s in error…the family they suggested the multicellular morph keys out in (Coelosphaerium) is prokaryotic, which is almost impossible to believe. I’m gonna try to hunt down one of their references tomorrow, see if they misread it.

Yes, this is from talkorigins and I am looking for verification.

the same issue was raised in 1996 on the ASA forum in response to Boxhorn’s comments. Boxhorn was a student of Boraas. He was an author of the second paper. In this faq the claim is not made so I think it wise to drop the claim myself.

Boxhorn email to ASA

I’ll see if I can Boraas to comment.

Comment #80287

Posted by Anton Mates on February 16, 2006 1:02 AM (e)

the same issue was raised in 1996 on the ASA forum in response to Boxhorn’s comments.

That’s where I noticed the objection, actually.

Just from looking at the Speciation FAQ list, it looks like the info would have come from one of the Journal of Phycology papers. Do you know if that’s the case?

Comment #80288

Posted by BlastfromthePast on February 16, 2006 1:39 AM (e)

There’s this statement from the paper: “Thirdly, … The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have beenmaintained for several months ….”

And then there’s this statement:
“This shows that active photosynthesis by the algae and continued interaction with the predator are essential to maintain the colonial algae in continuous culture.”

If you put the two statements together it seems to imply that the predator was present as well when the Chlorella “bred true” on the culture and agar.

If that were the case, then this doesn’t seem to rule out the possibility of the predator flagellate being the “inducer”: meaning that it interacts with chlorella, either directly or indirectly, bringing about a pre-packaged response in the Chlorella.

Another nagging question is whether or not the presence of the unicellular form of Chlorella is a trigger for going back to the unicellular form. If the predator is present in the culture/agar mediums, then even if the ‘inducer’ is absent, the signal to return to unicellular form–that is, the unicellular form of Chlorella–would never be present since it would be devoured by the predator. That’s why I think it’s important to know whether the predator was present during the two years of ‘breeding true.’

Further, it is clear that we’re not dealing with some kind of ‘pherome’ issuing from the predator that ‘induces’ the colonial form of Chlorella. But perhaps the “inducer” is something that is exuded/produced/spilt out from the dead prey. Or perhaps it’s something that the predator produces–excrement–that has some residual substance from the devoured Chlorella. (If the latter case holds, is this then why it takes 20 genertations before it switches over to the colonial form?) If that’s the case, then in the presence of the predator (1) the unicellular form will be triggered to go to the colonial form, and (2) in the continued presence of both unicellular Chlorella and predator, the colonial form will persist.

So, to me, it’s absolutely critical to know whether or not the predator was present when the colonial Chlorella was ‘breeding true’. And I think it would be great to run the experiment again, and this time, once colonization takes place to remove the predator and “flood” the colonial form with the unicellular form to see whether, indeed, the unicellular form does act as a trigger back to the unicellular form.

Comment #80289

Posted by sonofblast on February 16, 2006 2:15 AM (e)

blast

Social amoeba, a model organism for the colonial theory of metazoan evolution, are normally a free living animal that lives in forest soil. When food runs short they send out a chemical “call to arms” where millions converge and form a “slug”. Some of them then modify their cellular structure into hard cell walls to form a stalk that pushes up above the soil and others at the tip of the stalk become spores and are (hopefully) transported to a better food supply to continue the species.

The amoeba that form the stalk die. The process of forming a rigid cell wall is irreversible. The rest of slug, once the spore creation is finished, return to being free living cells for whatever fate awaits them (presumably starvation since that’s what triggered the slug formation in the first place).

I doubt like the algae evolved under the researcher’s nose. An environmental trigger caused the transition to colonial behavior sure as I’m sitting here writing this.

sob

Comment #80292

Posted by Anton Mates on February 16, 2006 2:24 AM (e)

BlastfromthePast wrote:

There’s this statement from the paper: “Thirdly, … The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have beenmaintained for several months ….”

And then there’s this statement:
“This shows that active photosynthesis by the algae and continued interaction with the predator are essential to maintain the colonial algae in continuous culture.”

If you put the two statements together it seems to imply that the predator was present as well when the Chlorella “bred true” on the culture and agar.

You’re misreading “continuous culture;” please look upthread at Pim’s description of same. Continuous culture uses a liquid medium, not agar. And when the first statement mentions liquid culture, it explicitly describes it as monospecific. One species: Chlorella. No flagellates.

Thus they showed that the multicellular morph breeds true in a variety of culture setups even when the flagellate predator is absent. It’s true that their second statement is slightly overgeneral–they mean you need the predator to maintain the colonial algae in continuous culture setups where there’s also a permanent source of unicellular Chlorella, either from a previous stage or (as is likely if this is the same chemostat where your multicellular morph originally popped up) as a small remnant population. That’s clear from their description of the two-stage chemostat in which the multicellular morph was seen to wash out. That morph disappears not because it reverts to a unicellular form but because such a culture already contains unicellular morphs which can now outcompete it.

Comment #80293

Posted by Anton Mates on February 16, 2006 2:44 AM (e)

sonofblast wrote:

The amoeba that form the stalk die. The process of forming a rigid cell wall is irreversible. The rest of slug, once the spore creation is finished, return to being free living cells for whatever fate awaits them (presumably starvation since that’s what triggered the slug formation in the first place).

In other words, the slug does not breed true. Both its spores and its remaining component cells after sporing are in the unicellular form. It doesn’t make more slugs.

The Chlorella multicellular morph, on the other hand, was shown to breed true. So no, this is mutation.

I doubt like the algae evolved under the researcher’s nose.

I’m sure you do.

Comment #80295

Posted by MP on February 16, 2006 3:21 AM (e)

Just some thoughts from a lurker…

If blast feels that an educated guess is no more valuable than a baseless guess, then I suggest he immediately cease using, and avoid future use of, any products that require extensive engineering, especially stuff that’s innovative. No planes, autos, computers, etc for you, M. Blast, because they were all designed using educated guesses, but we in the biz call it engineering judgment. Especially stay away from aircraft. I recall an aero-engineer once saying, “ After a hundred years of flying, we still don’t know exactly what makes a plane fly.” Just remember that the next time you jump on a plane, and pray to your designer that educated guesses really are more valuable than uneducated ones.

On a related note, blast said,”And I stand by my initial assessment: this phenomena is, plain and simple, an induced reaction by the chlorella in response to an environmental stimulus. Prove me wrong!”
Based on the above statement, my assessment is that thousands of invisible pixies carry planes to make them fly. Prove me wrong!

Comment #80372

Posted by BlastfromthePast on February 16, 2006 1:39 PM (e)

Anton:

I’m going to intersperse my comments among your last post. I think it’ll be tidier that way.

“Thus they showed that the multicellular morph breeds true in a variety of culture setups even when the flagellate predator is absent.

I’m not sure you read all my comments on the last post. One of the things I suggested is that it is the ‘presence’ of the unicellular form that triggers the decline in the colonial form. I know you address this down below–and I’ll respond to that portion below–but I just want to make sure you’re aware of the point I was suggesting.

It’s true that their second statement is slightly overgeneral—they mean you need the predator to maintain the colonial algae in continuous culture setups where there’s also a permanent source of unicellular Chlorella, either from a previous stage or (as is likely if this is the same chemostat where your multicellular morph originally popped up) as a small remnant population.

A question here: (not sarcastic) How do you know that’s what they mean? I don’t necessarily disagree; in other words, is there something I’ve missed? Now assuming what you say is actually the case, then the suggestion remains that the predator is needed to eliminate the presence of the unicellular form amongst the colonial form or else the colonial form will disappear. How do you respond?

That’s clear from their description of the two-stage chemostat in which the multicellular morph was seen to wash out.

It’s not clear to me (again, not sarcastic) because they seem to imply that the only reason the colonial form disappears is because of the absence of UV for photosynthesis. They don’t appear to mention any other reason.

That morph disappears not because it reverts to a unicellular form but because such a culture already contains unicellular morphs which can now outcompete it.

I’m not sure what you mean here. Is this just you’re impression (again, not sarcastic), or is there something that makes this clear? (BTW I’m working on the excerpts that have been posted here; I don’t have access to the article. Maybe you do. If so, is there a URL I can use?) Are you talking about the two-stage chemostat? If you are, again, isn’t the reason they die the absence of UV?

I think knowing the conditions under which the colonial form reverted is vital to the interpretation.

Comment #80384

Posted by Russell on February 16, 2006 2:27 PM (e)

sob wrote:

I doubt like the algae evolved under the researcher’s nose. An environmental trigger caused the transition to colonial behavior sure as I’m sitting here writing this.

Cool! we went from “I doubt…” (based on no reason at all) to “sure as I’m sitting here”. Think of all the money the NIH could save if we could just all achieve certainty that way!

Comment #80385

Posted by Henry J on February 16, 2006 2:28 PM (e)

Re “One of the things I suggested is that it is the ‘presence’ of the unicellular form that triggers the decline in the colonial form.”

A thought here: if the mix of unicell and multicell versions is now in an environment in which the unicell is more successful, then perhaps the multicell form declines simply because it is being outcompeted for the available resources? (I.e., not because of any conversion from one form to another one.)

Henry

Comment #80429

Posted by BlastfromthePast on February 16, 2006 5:55 PM (e)

Henry wrote: “A thought here: if the mix of unicell and multicell versions is now in an environment in which the unicell is more successful, then perhaps the multicell form declines simply because it is being outcompeted for the available resources? (I.e., not because of any conversion from one form to another one.)”

Can’t discount it. If there’s some interaction between predator and prey which ‘triggers’ the colonial form, and if the presence of a considerable amount of unicellular Chlorella ‘triggers’ the multicell to become unicell, then you have a situation where the unicell Chlorella will begin to take over once the predator is removed and as a result the multicell will decline–if the ‘trigger’ system really applies. So your left with trying to decipher if the decline is NS–i.e., the unicells have an advantage–or, if a signal has been sent. How do you distinguish?

I wonder if you could culture the unicell form, place in the dark until even the unicell died, and then take that solution and add it to a multicell culture and see how the multicell forms react. If, indeed, there’s a signal chemical/pherome of some sort, then it might just get the colonial form to decline in the absence of competition for nutrients with the unicells. But, of course, nothing might happen; the colonial form could just continue along; and then you don’t know what to conclude.

Comment #80434

Posted by Anton Mates on February 16, 2006 6:10 PM (e)

BlastfromthePast wrote:

I’m not sure you read all my comments on the last post. One of the things I suggested is that it is the ‘presence’ of the unicellular form that triggers the decline in the colonial form. I know you address this down below—and I’ll respond to that portion below—but I just want to make sure you’re aware of the point I was suggesting.

Actually, I did miss that. I’ll discuss that possibility down below.

It’s true that their second statement is slightly overgeneral—they mean you need the predator to maintain the colonial algae in continuous culture setups where there’s also a permanent source of unicellular Chlorella, either from a previous stage or (as is likely if this is the same chemostat where your multicellular morph originally popped up) as a small remnant population.

A question here: (not sarcastic) How do you know that’s what they mean? I don’t necessarily disagree; in other words, is there something I’ve missed?

I’m not sure, but it’s quite straightforward. They explicitly stated that you don’t need the predator to maintain the colonies on agar, nor to maintain the colonies in a monospecific continuous culture. They then give an example of a continuous culture which isn’t monospecific, but has both Chlorella morphs–the nitrogen-limited two-stage chemostat–and there you do need the predator to maintain the colonies. So it’s clear that the presence or absence of the unicellular morph is what determines whether the predator’s necessary to keep the colonies around. Colonies do fine with both, and fine with neither, but will disappear if their culture contains the former organism without the latter.

Now assuming what you say is actually the case, then the suggestion remains that the predator is needed to eliminate the presence of the unicellular form amongst the colonial form or else the colonial form will disappear. How do you respond?

According to the paper, the predator never actually eliminates the unicellular form, merely keeps it very rare. But yes, it’s definitely true that if the predator’s removed, the unicellular population rebounds and the multicellular form washes out. That’s exactly what the authors are saying.

It’s not clear to me (again, not sarcastic) because they seem to imply that the only reason the colonial form disappears is because of the absence of UV for photosynthesis. They don’t appear to mention any other reason.

Other factors are inherent in the chemostat setup. For an organism to “wash out” of a continuous culture does not imply that it simply dies–rather, it fails to reproduce quickly enough to offset the constant population loss as the used medium is drained away, and/or is outcompeted by any other organisms. Of course it could simply be outright dying from lack of light (not UV in particular as far as I know), but that’s pretty unlikely here–the researchers don’t suggest that that’s happening, and Chlorella’s mixotrophic (i.e. doesn’t have to photosynthesize to survive.)

The paper also says, “In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the light, the multicellular form was slowly displaced by unicells (data not shown). Hence, without the predator, unicells are superior competitors in our continuous culture system.” So unicellular Chlorella does slightly better than the colonial morph when there’s light, but a lot better than the colonial morph when there’s no light. That’s probably because, as discussed in the paper, unicellular Chlorella’s better at absorbing nutrients than the colonial morph (more surface area per cell). That advantage becomes more significant when the lights go out and the only way of getting energy is to absorb it from the medium in chemical form.

(BTW I’m working on the excerpts that have been posted here; I don’t have access to the article. Maybe you do. If so, is there a URL I can use?)

I doubt there’s a link available for the general public; I pulled the article through my university library website. You can often get reprints of individual articles from the author, though, if you contact them.

—-

Now, concerning your suggestion that the colonial morph is transformed back into the unicellular morph via induction, rather than being outcompeted: well, now we’ve got two hypothetical inducing substances, yes? Substance A, produced by the flagellate or its attacked prey, which promotes colonialism; and Substance B, produced by the unicellular morph all the time, which promotes unicellularity. Problems with this:

In order to square with the lengthy time it takes for colonies to appear the first time around, Substance A must only promote colonialism when it reaches a relatively high concentration. At the same time, it must force colonies to stay colonial even at low concentration, because the paper says, “the colonial growth form has been maintained in mixed-species cultures for over 2 years, even at low flagellate densities.” Substance B, meanwhile, must be completely unable to promote unicellularity as long as there’s any of Substance A around.

Furthermore, this effect must somehow completely reverse when the lights go out–now Substance A fails to maintain or induce colonialism as long as there’s any of Substance B around–because when the culture isn’t illuminated, the colonies disappear even though the flagellates are still around and munching on the unicellular form!

Furthermore, the increasing concentration of Substance A must somehow cause Chlorella to first clump into colonies of all sorts of sizes, then eventually settle on 8-cell colonies, as was seen in the study.

That’s a lot of ad hoc hypotheses. Could you throw enough of them together to account for this data via chemical induction? Probably. But it’s much more simply explained by random mutation + selection.

Comment #80435

Posted by Anton Mates on February 16, 2006 6:13 PM (e)

BTW, I was unable to find anything in the Journal of Phycology on keying out the colonial Chlorella morph, nor did I find anything like that in papers citing the Boraas papers. So if you get a reply, Pim, I’d love to hear it. Otherwise I guess I’ll write talk.origins and suggest that claim be taken out.

Comment #80436

Posted by Jason on February 16, 2006 6:28 PM (e)

i suppose that depends entirely on how valid you wish your point to be, and what that point intends to address.

If you want to address the grammar of the paper, you certainly don’t have to even be an english major, but if you want to critique the methods or conclusions of a scientific paper, your point is better made if you have studied the subject material, and understand at least how experiments in the subject matter at hand are designed.

saying to someone “test it yourself” is a slap at the fact that the persona it was directed at in fact has NO clue at all about algal physiology, ecology, or even how one goes about beginning to answer questions about same.

so what’s your point then?

that there are errors in the paper, or that internet commentary in general isn’t worth the time taken to type it?

My point is that this is an internet message board/blog, whatever.

This is not a journal editorial board. This isn’t even a scientific conference.

Any layman can make just about any statement (non offensive) about this paper that they want.

Then, another layman, or a person actually working in that field, may correct him to the best of their abilities.

But, “test it yourself” is a cop out. It doesn’t serve any purpose in the debate, if there is one. If you want to educate someone and think you can, try. “Test it yourself” serves no purpose in any debate on any internet message board.

Comment #80443

Posted by Jason on February 16, 2006 6:57 PM (e)

Anton wrote:

That said, I believe the multicellular morph would key out as a different species. Not only is it single-celled versus multicellular—a huge morphological difference in itself—but they observed other related differences between the two in terms of reliance on photosynthesis, success in low-nutrient environments and (obviously) resistance to predation. I’m no expert on defining species in asexual organisms, but I know they’ve been defined on much less than that.

I’ll just say that the colonies don’t realize they are a different species. And dogs don’t know it’s not bacon.

Anton wrote:

While it’s true that you apparently see colony formation pretty reliably when you repeat the experiment, that doesn’t mean “the ability to form colonies is just part of the genome.” It means that the genome can reliably be modified by mutation to gain that ability.

That’s why I suggested the type of experiment that the Boraas group could have started right after doing the ones they wrote up.

I’ll put money on it. I’ll bet that if you isolated a few individuals from the unicellular population and cultured those seperately to let the population get pretty high, then introduce the predator, you’d see a repeat of the previous results. I think that there would be colony formation and it would happen in a similar fashion.

Anton wrote:

And in turn that doesn’t mean that the genome is somehow set up to produce one particular mutation.

Not one particular mutation, but perhaps, a different type of gene expression. The expression and its effects might differ in degree among individual colonies. The 8-cell colonies eventually won out because they were the right blend of size and catabolic/metabolic efficiency.

You’ll notice that the actual genetic mechanism for colony formation must have differed somewhat between colonies, because there were a ton of different colony sizes at first before the eight-cell colonies won out. That suggests that lots of different mutations are possible which all result in various multicellular morphs.

We know that morphology is not 100% dependent on what genes are present, but are largely dependent on which genes are expressed and to what degree.

This might be the reason for all the variation in morphology.

You say above that the results of their experiment don’t mean something, and it’s true. They should have performed more experiments to try to flesh out the mechanism of colony formation. Is it something intrinsic to this species? Was it a mutation that occured in the very first rebound period that lasted 10-20 generations? They left some serious questions open and a few simple experiments (simple with the set-up they already had going) would shed some light on those questions.

Anton wrote:

The researchers just hit upon a study organism and a selection pressure which was remarkably well-suited to induce speciation.

I don’t think that they adequately demonstrated that there was indeed a speciation event. I don’t think they ruled out some mechanism that already existed for this species.

Comment #80448

Posted by Sir_Toejam on February 16, 2006 7:38 PM (e)

bloody pant-loading nonsense.

that’s exactly why we take a poke at these types of arguments.

they simply don’t EVER hold up when push comes to shove.

go find ANY reputable study that supports the idea of pant-loading.

we’ve been all through this with blast; remember front-loaded snake toxins, blast?

give it up, really.

Comment #80484

Posted by Anton Mates on February 16, 2006 11:24 PM (e)

Jason wrote:

I’ll just say that the colonies don’t realize they are a different species. And dogs don’t know it’s not bacon.

I…can’t argue with that. I think.

While it’s true that you apparently see colony formation pretty reliably when you repeat the experiment, that doesn’t mean “the ability to form colonies is just part of the genome.” It means that the genome can reliably be modified by mutation to gain that ability.

That’s why I suggested the type of experiment that the Boraas group could have started right after doing the ones they wrote up.

I’ll put money on it. I’ll bet that if you isolated a few individuals from the unicellular population and cultured those seperately to let the population get pretty high, then introduce the predator, you’d see a repeat of the previous results. I think that there would be colony formation and it would happen in a similar fashion.

They did do that, and colony formation did occur more often than not. “We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.”

You seem to believe that the repeatability of this effect implies that it can’t be speciation, but the two really have nothing to do with each other.

We know that morphology is not 100% dependent on what genes are present, but are largely dependent on which genes are expressed and to what degree.

This might be the reason for all the variation in morphology.

The expression of genes is dependent on what other genes (alleles) are present, though. A difference in gene expression is still a genetic difference.

Moreover, I notice that unicellular Chlorella stuck around, just in much smaller numbers. Which I like–I said earlier that I was hoping they could pull off a system with the morphs living side by side. That makes it a much better case for speciation–two morphs, in the same culture, occupying different niches.

You say above that the results of their experiment don’t mean something, and it’s true. They should have performed more experiments to try to flesh out the mechanism of colony formation. Is it something intrinsic to this species? Was it a mutation that occured in the very first rebound period that lasted 10-20 generations? They left some serious questions open and a few simple experiments (simple with the set-up they already had going) would shed some light on those questions.

Again, they repeated this many times. Colonies don’t show up every time, but they show up more often than not.

I don’t think that they adequately demonstrated that there was indeed a speciation event. I don’t think they ruled out some mechanism that already existed for this species.

That’s what the tests of true breeding were for, and they did that quite well.

Comment #80485

Posted by Anton Mates on February 16, 2006 11:32 PM (e)

The expression of genes is dependent on what other genes (alleles) are present, though. A difference in gene expression is still a genetic difference.

I should add to this, though, that I understand your argument that the initial boom and then decline in colony morphological variation could be partially evolution-based and partially induced. If there was a built-in mechanism that switched the cells over to colonial, that could expose previously hidden genetic variation, now expressed through their colony sizes and shapes; selection could then winnow most of these out.

However–independently of the other evidence the paper provided that there’s no such mechanism–I think you’d still expect comparatively little variation, since presumably the last time these cells’ ancestors had to go colonial, they went through the same sort of selection.

IOW if going colonial is just something Chlorella does from time to time via a built-in mechanism, and if selection acts to narrow down the range of colony sizes, then Chlorella colony sizes should already be narrowed-down due to past selection.

Comment #80486

Posted by Anton Mates on February 16, 2006 11:41 PM (e)

IOW if going colonial is just something Chlorella does from time to time via a built-in mechanism, and if selection acts to narrow down the range of colony sizes, then Chlorella colony sizes should already be narrowed-down due to past selection.

And an addendum to this in turn (I know, I’ll never stop):

An obvious counter to the above is to say, “Well, maybe different Chlorella in the culture are from different lineages, so their initially diverse colony sizes would reflect the diverse environments their various ancestors were in the last time they went colonial.” Which is possible. But I think it’s unlikely–cultures are usually inoculated with relatively small numbers of organisms, and the vicious competition in continuous cultures that I described earlier means that any lineage with a reproductive rate even slightly lower than others’ will wash out. Both factors suggest that the Chlorella in a mature culture are going to be mostly from the same lineage.

Comment #80628

Posted by Jason on February 17, 2006 7:29 PM (e)

I don’t know what pant-loaded means. It must be very techincal jargon.

Anton wrote:

They did do that, and colony formation did occur more often than not. “We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.”

I took that to mean that they harvested cells from the 30 year old culture multiple times. But, I guess, as long as they made sure that they harvested only unicells, then there’s no real difference.

Anton wrote:

You seem to believe that the repeatability of this effect implies that it can’t be speciation, but the two really have nothing to do with each other.

No, not necessarily. I just thought that if they harvested only a few unicells and cultured those and colonies still formed, that it might support the idea that this is a built-in genetic mechanism for this species. But really, now that I think about it again, it wouldn’t really support one hypothesis or the other. It could be built in or the same type of mutation occurs readily and repeatably.

I know it would cost major bucks, but maybe they should try to map the genome of the unicells and the colonies to see what the differences may be if any. That would probably be the most definitive way to tell what happened.

Anton wrote:

The expression of genes is dependent on what other genes (alleles) are present, though. A difference in gene expression is still a genetic difference.

Well, correct me if I’m wrong, but I was under the impression that one of the drawbacks to cloning is that the chemical environment in the cloned “zygote” is not identical to what it would be in a normal zygote. The genes are practically identical to the genes that the “mother” of the clone had when they were concieved, but the expression of those genes is different just because of the slightly different chemical environment. The clone has a few deficiencies because of this.

All I am saying is that there doesn’t always have to be a difference in the genes for there to be a difference in gene expression.

I don’t think that they adequately demonstrated that there was indeed a speciation event. I don’t think they ruled out some mechanism that already existed for this species.

That’s what the tests of true breeding were for, and they did that quite well.

Ok, if true breeding is what defines a species, then so be it.

Would a conjoined twin with one set of gonads “breed true”? I wouldn’t think so.

I imagine that each cell in the colony divides though, is that right?
And what buds off of each colony is a new intact colony?

I really think they should propose mapping the genome before and after, even doing it for a few different colonies. That’s probably too much to ask, but it really would shed a whole lot more light on this.

Anton wrote:

IOW if going colonial is just something Chlorella does from time to time via a built-in mechanism, and if selection acts to narrow down the range of colony sizes, then Chlorella colony sizes should already be narrowed-down due to past selection.

Why are you so sure of that? Why should it do what you think it should “by now?”

Anton wrote:

An obvious counter to the above is to say, “Well, maybe different Chlorella in the culture are from different lineages, so their initially diverse colony sizes would reflect the diverse environments their various ancestors were in the last time they went colonial.” Which is possible. But I think it’s unlikely—cultures are usually inoculated with relatively small numbers of organisms, and the vicious competition in continuous cultures that I described earlier means that any lineage with a reproductive rate even slightly lower than others’ will wash out. Both factors suggest that the Chlorella in a mature culture are going to be mostly from the same lineage.

Well, it wasn’t so obvious to me, so thanks.

Even with a few or even one strong lineage, I don’t know why there would be any reason to be so certain that “going colonial” would have reached such a high level of efficiency that only eight-celled ones are formed. If Chlorella had only one predator, then maybe, but if there are many different types of predator, then many different colony sizes would be favorable and perhaps in the case of a larger or more capable predator colonies of 16 cells might be ideal. For a smaller one, maybe four cells would turn out to work the best. I don’t know.

BTW - thank you for your candor in all of this. This is all very interesting and I’m learning a lot.

Comment #80636

Posted by Jason on February 17, 2006 8:38 PM (e)

Something just dawned on me.

They said they reproduced the experiment many times and got 8-celled colonies about 70% of the time.

Does that mean that each one of those cultures with 8-celled colonies represents a new species? So that there are many many different species of 8-celled colonies? Or did mutation and selection converge on the same species time and time again? That seems highly unlikely (notice I didn’t use the ID line of it’s so unlikely as to be impossible since that’s BS.)

Comment #80648

Posted by PvM on February 17, 2006 11:10 PM (e)

Anton Mates seems to have answered most if not all objections by Blast and Jason. If I have missed any please repeat them. Yes, the multicellular form remains multicellular even away from the predator. The confusion may have been when discussing the dual stage chemostat experiment where the two forms do compete.

Interesting tidbit is that the original paper was based on an experiment where the second stage which contained the predator backflushed into the primary system, which almost by chance led to an interesting experiment. Even if the two are still considered the same species, the step from single to multicellular should be seen as a major innovation.

Comment #80661

Posted by Anton Mates on February 18, 2006 2:29 AM (e)

Jason wrote:

I know it would cost major bucks, but maybe they should try to map the genome of the unicells and the colonies to see what the differences may be if any. That would probably be the most definitive way to tell what happened.

It would be, though of course you’d have to rule out all the other irrelevant genetic variations you’d find. I think Boraas himself has gone on to related things, like some work with algae and rotifers–his general interest seems to be evolution due to predator-prey arms races. I dunno anything about the guy personally, but his lab sounds like the place to be if you’re interested in working on this stuff.

Well, correct me if I’m wrong, but I was under the impression that one of the drawbacks to cloning is that the chemical environment in the cloned “zygote” is not identical to what it would be in a normal zygote. The genes are practically identical to the genes that the “mother” of the clone had when they were concieved, but the expression of those genes is different just because of the slightly different chemical environment. The clone has a few deficiencies because of this.

All I am saying is that there doesn’t always have to be a difference in the genes for there to be a difference in gene expression.

Ah, yeah, I see. That’s certainly true–actually it comes up in locusts, which are a good example of “fake evolution.” You probably know how a single locust species switches between the solitary phase and the gregarious phase–the latter being when they’re really “locusts,” swarming around and eating all the vegetation wherever they land. The switch is triggered by crowding, and it takes something like three generations to complete, so it looks kind of like super-rapid evolution in response to the crowding environment. (But we know it’s not, because every offspring of a crowded solitary-phase grasshopper looks more like the gregarious phase. Whereas if it was real mutation & selection we’d see just a couple of offspring look like that, who would then outcompete the ordinary solitary-phase ones in later generations. Plus the same thing happens in reverse if you put gregarious-phase grasshoppers by themselves; they don’t breed true.)

But anyway, the grasshopper offspring do “inherit” the same phase as their mother, only it’s not genetic–it’s due to hormones their mother packed the egg with, that continue to influence the embryo in development. So yeah, that’s an example of non-genetically-determined gene expression.

Ok, if true breeding is what defines a species, then so be it.

Would a conjoined twin with one set of gonads “breed true”? I wouldn’t think so.

It’s more that true breeding defines the lines between species, because it shows that organism A isn’t just a temporary form of organism B; it’s apparently going to just be A forever. In sexual species there’s also rules about little or no gene flow–hybrids should die or be sterile, that kind of thing–but Chlorella’s obligately asexual AFAIK.

So if the conjoined twin can, say, self-fertilize and make more conjoined twins, I guess it’s a species! But it kind of has to be around for a while before people bother calling it a species as opposed to “that freaky thing our study found.” For instance no one bothers calling most cancer cells separate species, but the HeLa lineage has survived so long (half a century after it killed Henrietta Lacks) and been so spectacularly successful in the culture environment that it’s often called Helacyton gartleri. It’s happily doing its thing and is obviously never going to turn back into a human and breed with us again.

I imagine that each cell in the colony divides though, is that right?
And what buds off of each colony is a new intact colony?

I’m not sure, from their description.

“Individual cells of the colony grew in size while dividing into daughter cells; the new colony then separated from the original colony by tearing or breaking the original mother cell wall.”

From the pictures attached, it looks like each cell divides into its own small 8-celled colony, then the parent colony breaks apart to produce 8 small colonies, whose cells then grow to full size.

IOW if going colonial is just something Chlorella does from time to time via a built-in mechanism, and if selection acts to narrow down the range of colony sizes, then Chlorella colony sizes should already be narrowed-down due to past selection.

Why are you so sure of that? Why should it do what you think it should “by now?”

Simply because it took such a short time to narrow it down in this study–a few weeks between the appearance of lots of sizes and the dominance of the 8-celled colony. Selection’s probably stronger in a chemostat environment, but presumably the ancestral Chlorella would have racked up a lot more than a few weeks in the colonial form.

An obvious counter to the above is to say, “Well, maybe different Chlorella in the culture are from different lineages, so their initially diverse colony sizes would reflect the diverse environments their various ancestors were in the last time they went colonial.” Which is possible. But I think it’s unlikely—cultures are usually inoculated with relatively small numbers of organisms, and the vicious competition in continuous cultures that I described earlier means that any lineage with a reproductive rate even slightly lower than others’ will wash out. Both factors suggest that the Chlorella in a mature culture are going to be mostly from the same lineage.

Well, it wasn’t so obvious to me, so thanks.

Heh. Gotta argue with myself when no one else is about.

Even with a few or even one strong lineage, I don’t know why there would be any reason to be so certain that “going colonial” would have reached such a high level of efficiency that only eight-celled ones are formed. If Chlorella had only one predator, then maybe, but if there are many different types of predator, then many different colony sizes would be favorable and perhaps in the case of a larger or more capable predator colonies of 16 cells might be ideal. For a smaller one, maybe four cells would turn out to work the best. I don’t know.

True, a varied environment could select for a balanced population of various morphs. But the colonies bred true for size as well–so barring some implausibly intelligent mechanism within Chlorella to actually detect the edible size range of a given predator and change colony size accordingly, each lineage would have an inherited particular colony size.

BTW - thank you for your candor in all of this. This is all very interesting and I’m learning a lot.

No problem. I have to be candid when I’ve never taken a class on this stuff, or for that matter taken an intro biology class since high school. I know I’ll be embarrassingly wrong fairly frequently.

Something just dawned on me.

They said they reproduced the experiment many times and got 8-celled colonies about 70% of the time.

Does that mean that each one of those cultures with 8-celled colonies represents a new species? So that there are many many different species of 8-celled colonies? Or did mutation and selection converge on the same species time and time again? That seems highly unlikely (notice I didn’t use the ID line of it’s so unlikely as to be impossible since that’s BS.)

Kind of a little of both, I suppose. We assume on statistical grounds that the exact set of mutations in each culture would be different, but it’s possible (as you mention above) that particular mutations leading to an N-cell colony show up in different cultures. Or, more likely from what I know of genetics, there’s a set of different possible mutations within a single gene that all have the effect of, say, inactivating it, leading to the same mutant phenotype of an N-cell colony. Would you call them all the same species in the latter case? I really don’t know, but I kinda think the phycologists (if that’s the right term) would. Identical phenotype, and genotypes very similar except for this one particular set of mutations. You’d probably just chalk them down as “intraspecific genetic variation.” But again, I’m not a systematist and this sounds like the kind of problem they just love to debate.

Anyway, whatever mutations happen in a particular culture, the ones leading to 8 (or occasionally 4) cells apparently always win out in the end. That’s actually not surprising given the standardized selection pressures–as they explain in the paper, an 8-celled colony is just bigger than the biggest objects the predatory flagellate will consume. (They tested this with plastic beads of various sizes.) Now add to that the fact that bigger colonies have more trouble absorbing nutrients, because their per-cell-volume surface area is smaller, and you can see why the 8-cell form win out. It doesn’t get eaten, unlike the smaller forms, and it’s better at feeding than the larger forms.

A cool way to check this hypothesis would be to find a different predator that has a different size range of accepted prey, and see if the final colony size is again just big enough to be out of that range. The paper does discuss several other cases (not necessarily mutation and selection, and some known to be built-in induced mechanisms) where single-celled prey organisms react to predation by clumping or chaining or developing long filaments and things that (under the microscope) seem to make it too hard for the predator to fully engulf them.

It also suggests a reason why multicellularity’s much more popular in eukaryotes than prokaryotes; the former have a larger minimum size, I suppose due to their various organelles. Whereas prokaryotes can avoid predation by being too small for many single-celled predators (the paper cites instances of this), eukaryotes can’t do that and their only option’s to get too big instead, by clumping up.

Eugh…Pim’ll have to take over. I have to go write something and get graded on it for once.

Comment #80664

Posted by BlastfromthePast on February 18, 2006 3:56 AM (e)

Anton Mates wrote:

Now, concerning your suggestion that the colonial morph is transformed back into the unicellular morph via induction, rather than being outcompeted: well, now we’ve got two hypothetical inducing substances, yes? Substance A, produced by the flagellate or its attacked prey, which promotes colonialism; and Substance B, produced by the unicellular morph all the time, which promotes unicellularity.

That’s not how I see it. There are three substances A, B, and C. A is produced by the unicells in an on-going manner. B is produced either by the dying algae directly, or in conjunction with the predator. Substance B then in turn causes substance C to be produced, which is the ‘trigger’ for the colonial form of the algae.

Problems with this:

In order to square with the lengthy time it takes for colonies to appear the first time around, Substance A must only promote colonialism when it reaches a relatively high concentration. At the same time, it must force colonies to stay colonial even at low concentration, because the paper says, “the colonial growth form has been maintained in mixed-species cultures for over 2 years, even at low flagellate densities.” Substance B, meanwhile, must be completely unable to promote unicellularity as long as there’s any of Substance A around.

I don’t see the problem if you think of this in terms of an ‘on/off’ switch. Unicell Chlorella prefers the unicellular form (as you tell it, the paper says that the unicellular form is more efficient in absorbing light and nutrients than the colonial form) and normally is producing substance A. Along comes the predator, substance B is produced, and the Chlorella ‘switch over’ to producing substance C. It’s not the case that the Chlorella are producing both A and C on a proportional basis, rather, when B is high enough (think in terms of the activation energy needed for chemical reactions) the Chlorella starts producing C alone. Now you have to think in terms of an ‘activation energy’ again for the Chlorella to go back to producing substance A again. So, being that there is a switch mechanism, once the colonial form is established, AND, in a ‘monospecific’ environment, it will keep on being colonial. Only in the presence of very high A will the colonial form ‘switch back’ to producing unicellular forms and substance A (rather than C). [There is a presumption that the Chlorella is more sensitive to the A signal than the C signal, so that where both are present in relatively equal amounts, the A signal will prevail] Where does the ‘very high’ A come from? It comes from some nearby area where the presence of the predator is low, or almost completely absent; and this ‘substance A producing area’ then spreads until it comes into contact with the colonial form, at which point, the Chlorella go back to the unicellular form. So then, likewise, in the presence of a predator, high concentrations of B are produced, the Chlorella ‘switch over’, and at a high enough concentration of B, spread over a large enough area (encompassing an exceedingly large number of Chlorella),the colonial form begins to take hold, and then this ‘substance C producing area’ begins to spread.

Furthermore, this effect must somehow completely reverse when the lights go out—now Substance A fails to maintain or induce colonialism as long as there’s any of Substance B around—because when the culture isn’t illuminated, the colonies disappear even though the flagellates are still around and munching on the unicellular form!

It’s clear from the article that the reason for the colonial form to ‘wash out’ was the lack of light. In a low-light situation, the colonial form might not survive well at all. In fact, I wouldn’t be surprised if the colonial form didn’t arise even in the presence of the predator unless there was a high level of light available. So you don’t have a situation in the two-stage chemostat where a ‘substance A producing area’ could spread—whatever amount of A that was being produced by the unicells in the first stage was diluted by the C being produced by those surviving unicells in the presence of the predator in stage two.

Furthermore, the increasing concentration of Substance A must somehow cause Chlorella to first clump into colonies of all sorts of sizes, then eventually settle on 8-cell colonies, as was seen in the study.

There is nothing that says some other sort of signaling takes place whereby the colonial Chlorella, sensing the environment that they’re in, settle on an appropriate cell-number. I think it would be easy to design experiments around this thesis. Nonetheless, I would think there would be some preferred sizes—just from the physics of the whole thing.

That’s a lot of ad hoc hypotheses. Could you throw enough of them together to account for this data via chemical induction? Probably. But it’s much more simply explained by random mutation + selection.

My impression is that you have this thing entirely backwards. As I’ve explained it, we’re dealing with signaling mechanisms, switching mechanisms, and high thresholds for the ‘switching.’ This simply sounds like an ‘engineered’ system. But we see all kinds of instances where biological forms exhibit ‘design.’ So that’s not surprising. But to think that RM+NS will operate in a repeatable fashion (this phenomena reappears 70% of the time) means that the right mutation has to occur at the right place, at the right time, 70% of the time.
If you went to Las Vegas and one of the dice you were rolling came up as a ‘six’ 70% of the time, what would you think? And it goes without saying that biological forms are a bit more complex than a die.
I don’t think the argument stands up to scrutiny here.

Comment #80680

Posted by PvM on February 18, 2006 7:50 AM (e)

But to think that RM+NS will operate in a repeatable fashion (this phenomena reappears 70% of the time) means that the right mutation has to occur at the right place, at the right time, 70% of the time.

You may misunderstand evolutionary theory here. Mutations do not happen because they are needed but rather mutations are present in the original stock and are selected for. And such rare variations of multicell cluseters were occasionally observed. Same with the peppered moth, darker forms were already present although seldomly seen. If it were induction you would expect a much better repetition behavior, you would not expect the maintenance of the form outside the presence of the predator where you now have to wait for a mutation to arise to return to the unicellular state.

In other words, the evidence points strongly against your hypothesis but as you say, you may think of ways to test it.

As I and others have explained, the much simpler explanation of variation and selection is much better explained by the observations.

Comment #80739

Posted by PvM on February 18, 2006 4:44 PM (e)

Another blow to the induction hypothesis presented by Blast

Secondly, once it has appeared, the colonial growth form has been maintained in mixed-species cultures for over 2 years, even at low ¯agellate densities.

Comment #80765

Posted by Anton Mates on February 18, 2006 7:01 PM (e)

BlastfromthePast wrote:

That’s not how I see it. There are three substances A, B, and C. A is produced by the unicells in an on-going manner. B is produced either by the dying algae directly, or in conjunction with the predator. Substance B then in turn causes substance C to be produced, which is the ‘trigger’ for the colonial form of the algae…..

I don’t see the problem if you think of this in terms of an ‘on/off’ switch. Unicell Chlorella prefers the unicellular form (as you tell it, the paper says that the unicellular form is more efficient in absorbing light and nutrients than the colonial form) and normally is producing substance A. Along comes the predator, substance B is produced, and the Chlorella ‘switch over’ to producing substance C. It’s not the case that the Chlorella are producing both A and C on a proportional basis, rather, when B is high enough (think in terms of the activation energy needed for chemical reactions) the Chlorella starts producing C alone. Now you have to think in terms of an ‘activation energy’ again for the Chlorella to go back to producing substance A again. So, being that there is a switch mechanism, once the colonial form is established, AND, in a ‘monospecific’ environment, it will keep on being colonial. Only in the presence of very high A will the colonial form ‘switch back’ to producing unicellular forms and substance A (rather than C). [There is a presumption that the Chlorella is more sensitive to the A signal than the C signal, so that where both are present in relatively equal amounts, the A signal will prevail] Where does the ‘very high’ A come from? It comes from some nearby area where the presence of the predator is low, or almost completely absent; and this ‘substance A producing area’ then spreads until it comes into contact with the colonial form, at which point, the Chlorella go back to the unicellular form. So then, likewise, in the presence of a predator, high concentrations of B are produced, the Chlorella ‘switch over’, and at a high enough concentration of B, spread over a large enough area (encompassing an exceedingly large number of Chlorella),the colonial form begins to take hold, and then this ‘substance C producing area’ begins to spread.

Chemostats are constantly stirred, and Chlorella has to be aerated. There aren’t going to be slowly spreading areas of “high concentration.” Moreover, colonial Chlorella is maintained even in cultures that have low predator densities and some of the unicellular morph.

It’s clear from the article that the reason for the colonial form to ‘wash out’ was the lack of light. In a low-light situation, the colonial form might not survive well at all. In fact, I wouldn’t be surprised if the colonial form didn’t arise even in the presence of the predator unless there was a high level of light available. So you don’t have a situation in the two-stage chemostat where a ‘substance A producing area’ could spread—whatever amount of A that was being produced by the unicells in the first stage was diluted by the C being produced by those surviving unicells in the presence of the predator in stage two.

Wait, what? The situation we have is that the colonials arise in the second stage when the lights are on, and disappear (and are replaced by single cells which are known to be descendants of the first stage, because of their smaller size) when the lights are off. Are you saying that when the colonials disappear, that is evolution in this particular case?

There is nothing that says some other sort of signaling takes place whereby the colonial Chlorella, sensing the environment that they’re in, settle on an appropriate cell-number.

Good God. More hypothetical signals? Substances A,B and C plus whatever internal chemical arrays lead to switchover hysteresis (your “activation energies”) plus light-sensitivity plus some other chemical network whereby the Chlorella all get together and agree that, yes, because this particular flagellate can’t eat eight cells, they should all switch over to that?

This is simpler and more plausible and testable than, “There were some mutations, and some of them were favorable?”

I think it would be easy to design experiments around this thesis.

How? What possible results could you get that couldn’t be dismissed with, “Well, there’s probably even more signaling mechanisms that account for whatever happened this time?”

Nonetheless, I would think there would be some preferred sizes—just from the physics of the whole thing.

What they found, repeatedly, is that there aren’t preferred sizes until several generations have passed. Initially there’s a ton of colony sizes. After a while, there’s only one or two. And the physics doesn’t change in that time period.

But to think that RM+NS will operate in a repeatable fashion (this phenomena reappears 70% of the time) means that the right mutation has to occur at the right place, at the right time, 70% of the time.

Nope, that’s neither what the data suggests nor what an evolutionary explanation requires. 70% of the cultures ended up mostly eight-celled–that simply means that one of the right mutations or combos of mutations has to occur in one of the millions of cells in 70% of your cultures. And as Pim points out, “the right time” just means “any time in the history of the culture before now.” Of course a colonial morph in the culture before the flagellate was introduced might well wash out, but the eight-celled forms usually didn’t appear until anywhere from forty to eighty generations after the introduction.

Given typical measured mutation rates, that implies literally millions of random mutations in the coding regions of the Chlorella genome–even if we ignore mutations that occurred before the flagellate was introduced. And just one of them needs to produce an 8-celled form by some not-horribly-debilitating mechanism.

Furthermore, the 8-cell form need not arise directly; almost any colonial morph is initially selected for, since any colony with more than 4 cells doesn’t get eaten. So if a 16-cell morph happens to arise first, it’s likely to stick around and possibly evolve to an 8-celled form a few generations later.

If you went to Las Vegas and one of the dice you were rolling came up as a ‘six’ 70% of the time, what would you think? And it goes without saying that biological forms are a bit more complex than a die.

If I’m rolling a million dice at once and at least one of them comes up as a six 70% of the time? I’m not gonna be too surprised. Heck, let’s make it more accurate and have me be a D&D freak who’s rolling with hundred-sided dice…I’m still not gonna be too surprised.

Comment #80811

Posted by BlastfromthePast on February 18, 2006 9:52 PM (e)

Sir Toejam wrote:

we’ve been all through this with blast; remember front-loaded snake toxins, blast?

give it up, really.

Gene recruitment, properly understood, basically means that there is no gene for Cobra venom, but a series of genes that are producing proteins in places that don’t normally produce proteins–like in salivary glands instead of the liver–and in great quantities. This is fully conformable to ‘front-loading’. No problem at all. ;)

And,BTW, there isn’t anything to “give up”, you see.

Comment #80813

Posted by PvM on February 18, 2006 10:07 PM (e)

This is fully conformable to ‘front-loading’. No problem at all. ;)

Anything is ‘conformable’ to front loading. After all we can look back in time and see how a particular feature evolved and thus claim ‘front loaded’. As such the argument of front loading remains fully scientifically vacuous although it at least allows religion to be reconciled with science.
I know that Mike Gene is a fan of this concept but he has yet to address how he intends to establish the concept of “front loading”. After all, there is a simpler explanation which looks at the same data but omits the ‘front loading’ part.

Comment #80815

Posted by Sir_Toejam on February 18, 2006 10:28 PM (e)

Gene recruitment, properly understood, basically means that there is no gene for Cobra venom, but a series of genes that are producing proteins in places that don’t normally produce proteins—like in salivary glands instead of the liver—and in great quantities. This is fully conformable to ‘front-loading’. No problem at all. ;)

amazing.

utterly, amazing.

we spent a whole week thoroughly trashing your argument, posting the relevant literature, even pulling in an expert on snake toxins to show you how your interpretations was simply, wrong.

I myself painstakeingly walked you through what was wrong with your argument, and why the articles you were citing in support of your pant-loading were actually perfect evidence in support of standard evolutionary theory….and here you just repeat yourself as if none of that ever happened.

do you wonder why we think you as nutty as larry?

do anybody else wonder now why those who actually DO science get so frustrated with folks like Larry and Blast?

Surely even you can see the similarities in your “presentations”?

It’s like beating your head on a rock, literally.

Comment #80819

Posted by steve s on February 18, 2006 10:53 PM (e)

do anybody else wonder now why those who actually DO science get so frustrated with folks like Larry and Blast?

I don’t think you have to get frustrated with them. I used to get frustrated all the time with such people, but then I took a step back. I realized that the math students I tutored can learn things if they want to, but if they refused to believe me, I couldn’t have taught them anything. I realized that if even 1% of the population was stubbornly ignorant, that was several thousand people in my city alone. No way can I make a dent in that by arguing with them, even if I work at it full time. So if they must exist, why should I let their existence affect me negatively? Afterward, I started looking at conversation situations in terms of, ‘what can I achieve? how much work will it take?’. I never get frustrated now because I never pin my hopes on futile arguments.

Comment #80821

Posted by 'Rev Dr' Lenny Flank on February 18, 2006 11:03 PM (e)

Gene recruitment, properly understood, basically means that there is no gene for Cobra venom, but a series of genes that are producing proteins in places that don’t normally produce proteins—like in salivary glands instead of the liver—and in great quantities. This is fully conformable to ‘front-loading’. No problem at all. ;)

Um, Blast, we already had the Snake Venom Guy here to tell you that you’re full of crap.

Or are you hoping everyone has forgotten?

Comment #80830

Posted by Anton Mates on February 18, 2006 11:51 PM (e)

Sir_Toejam wrote:

do you wonder why we think you as nutty as larry?

Oh, I certainly don’t. Larry is certifiable. He has many detailed and extremely odd ideas about the world, and absolutely no understanding of what other people will think of them or his actions. But Blast’s quite sane–he simply doesn’t actually aim to understand natural phenomena. His sole objective is to argue against evolution as strongly as possible. I’m not sure if this is on religious grounds or simply for personal entertainment. (Which isn’t an insult–everyone loves a good argument, right? I certainly do. I just think this is too important a topic not to get right.)

You can’t really hope to change either’s mind by talking to them, but I think some discussions with Blast are worthwhile simply because he usually makes not-completely-insane arguments whose refutation is a good mental exercise (and hopefully informative for those few people who know even less about this subject than I do.)

Comment #80832

Posted by BlastfromthePast on February 19, 2006 12:24 AM (e)

RD Lenny Flank wrote:

Um, Blast, we already had the Snake Venom Guy here to tell you that you’re full of crap.

Or are you hoping everyone has forgotten?

And you’ll remember that the Snake Venom Guy never gave me a direct answer to my question about gene recruitment. So I had to go looking for myself. And I actually got into correspondence with the guy who wrote the orginal article on gene recruitment. And, I’ve had time to digest it all a little bit. And, as I wrote in the earlier post, there’s really no such thing as a Cobra venom gene–that’s why they had to come up with the term ‘gene recruitment’. So, Lenny, you’ll just have to come up with some other objection to ‘front-loading’.

Sleep tight.

Comment #80838

Posted by Sir_Toejam on February 19, 2006 3:10 AM (e)

And you’ll remember that the Snake Venom Guy never gave me a direct answer to my question about gene recruitment.

sure about that? I think your memory is rather selective on the issue. he did indeed answer whatever relevant questions you presented.

why don’t you post a link back to that thread so anybody interested can see for themselves, eh?

Comment #80849

Posted by 'Rev Dr' Lenny Flank on February 19, 2006 8:06 AM (e)

Syntax Error: mismatched tag 'quote'

Comment #80851

Posted by 'Rev Dr' Lenny Flank on February 19, 2006 8:07 AM (e)

And you’ll remember that the Snake Venom Guy never gave me a direct answer to my question about gene recruitment. So I had to go looking for myself. And I actually got into correspondence with the guy who wrote the orginal article on gene recruitment. And, I’ve had time to digest it all a little bit. And, as I wrote in the earlier post, there’s really no such thing as a Cobra venom gene—that’s why they had to come up with the term ‘gene recruitment’. So, Lenny, you’ll just have to come up with some other objection to ‘front-loading’.

Sleep tight.

Here, Blast, let me remind everyone what Dr Fry said about your “frontloading” crap:

As I mentioned before, venom toxins are NOT modified salivary proteins. Rather they are the mutation of a normal body protein for the use as a toxin. There is not a magic little amino acid sequence added on but rather changes to existing functional residues or rearrangement of molecular scaffold. All of which is new information as this is occuring on a duplicate gene to the normal body protein, not to the body protein itself.

Venom evolution is much easier to understand if you follow the data trail rather than trying to shoe-horn it into a prepackaged theory that is particularly useless.

In other words, read the papers I’ve already referenced above.

Read those papers yet, Blast?

Or do you prefer to get your, uh, science information from “ecological visionaires”. (snicker) (giggle)

Comment #81283

Posted by BlastfromthePast on February 21, 2006 4:27 PM (e)

Sir Toejam wrote:

sure about that? I think your memory is rather selective on the issue. he did indeed answer whatever relevant questions you presented.

RD Lenny Flank wrote:

Read those papers yet, Blast?

Indeed, I did read those papers. It was ‘those papers’ that the good Dr. referred me to when I asked about ‘gene recruitment.’ In those papers, you’ll find intimations as to what gene recruitment is, but no more; not enough to give you a full idea of what it involves. Ultimately, I got in touch with the scientist who was the first to write about ‘gene recruitment’. He gave me access to his paper (only the ‘abstract’ was online) and that answered my questions for the most part.

As to his opinion of ‘front-loading’: well, that’s his opinion: he’s a Darwinist; what would you expect?

But let’s look a little at the facts: as I remember it, venom production involves the ‘gene recruitment’ of 8-10 ‘genes’. From a Darwinian perspective, there are then 8-10 recruitment events that you have to explain, as well as the timing of those events (it’s fair to assume there may have been simultaneous gene recrutiment of all 8-10 ‘genes’); whereas, with the ‘front-loading’ hypothesis you can simply assume that some ‘swithch’ for ‘gene recruitment’ was ‘switched on’ that affected all 8-10 proteins at once. Much simpler, neater.

Comment #81296

Posted by Sir_Toejam on February 21, 2006 5:19 PM (e)

But let’s look a little at the facts:

facts? I’ve NEVER seen anything from you but your selective interpretations, not based on anything in reality.

Is it really the best you could do to read the abstract of the key paper you were referenced?

pathetic.

give me ONE good reason why any of us should bother to listen to anything you have to say, when you entirely dismiss all of the scientific arguments as:

As to his opinion of ‘front-loading’: well, that’s his opinion: he’s a Darwinist; what would you expect?

*sigh*

you are a complete buffoon.

Comment #81319

Posted by 'Rev Dr' Lenny Flank on February 21, 2006 6:41 PM (e)

Indeed, I did read those papers.

No you didn’t, you liar.

Comment #81352

Posted by BlastfromthePast on February 21, 2006 9:49 PM (e)

Sir Toejam wrote:

Is it really the best you could do to read the abstract of the key paper you were referenced?

pathetic.

Try reading the post again. You’ll notice that I said all I could find was the abstract–you either had to pay for the article or have had a subscription to the service; I cared to do neither. I later got the original article from the good Dr. himself. Gracious man.

RDLenny Flank wrote:

BlastFTPast wrote:

Indeed, I did read those papers.

No you didn’t, you liar.

Lenny, what do you call a person who, without any basis at all, chooses to slander someone else? Whatever the label/word is, look in the mirror. That’s you.

Comment #81369

Posted by 'Rev Dr' Lenny Flank on February 21, 2006 10:43 PM (e)

No you didn’t, you liar.

Lenny, what do you call a person who, without any basis at all, chooses to slander someone else?

You didn’t read a single one of them. Not a one. None. Zip. Zero. Zilch. Nada. Not a one.

You are a liar, Blast. That is not “slander”. That is a simple statement of observable fact. You lie. That makes you a liar.

(shrug)

Comment #81380

Posted by Sir_Toejam on February 21, 2006 11:11 PM (e)

He gave me access to his paper (only the ‘abstract’ was online) and that answered my questions for the most part.

you are correct, Blast. I misread that.

well, I’m sure you understand the confusion, since you never actually read 99% of the papers that are referred to you (beyond the abstracts)…. and don’t claim any righteous indignation, as i can find the relevant passages, where you stated how you only could get the abstracts, just like you did above.

the reason lenny calls you a liar, is that he knows well that your extremely limited understanding of the principles behind the referenced papers make them well beyond your ability to elucidate any substantive errors either in method or conclusion.

so while you technically may have “read” the papers in question, no doubt your comprehension would be the equivalent of an elementary school childs “reading” of them.

this is the level of understanding of the priniciples and methods you have exhibited over and over again, and the reason we kept referring you to more basic texts to fill in your knowledge of the subject material.

which of course you completely ignored in favor of your own perceptional viewpoint.

look, Blast, last time here…

your problem is that you can’t have a realistic viewpoint on an issue you understand so little about.

a 3 year old might have an entirely entertaining view on why the sky is blue, but without knowledge of how light refraction works, and an idea of the molecular composition and organization of the atmosphere, that idea isn’t really worth listening to, is it.

That’s what I’m saying, Blast. You have consistently exhibited a gross lack of knowledge of the relevant background information needed to parse the data in the articles referenced.

go back to school and learn a few basic bits before launching into unfounded attacks on things you clearly misunderstand.

afterwards, when you can exhibit at least some knowledge of the topics involved, i won’t be asking you questions like “why should we bother to listen to anything you have to say?”

As python would put it:

“you don’t have to Go Leaping for the clitoris like a bull at the gate.”

now go away you irritating buffoon.

Comment #81387

Posted by 'Rev Dr' Lenny Flank on February 21, 2006 11:45 PM (e)

so while you technically may have “read” the papers in question, no doubt your comprehension would be the equivalent of an elementary school childs “reading” of them

Bah. He didn’t read a one of them. He’s a damn liar.

And anyone like him who gets his, uh, “science information” from self-styled “ecological visionaries” that he finds through Google, is not only a liar, but a pig-ignorant clod, too.

Blast simply isn’t worth listening to. He’s a braying jackass. Nothing more. (shrug)

Comment #81643

Posted by BlastfromthePast on February 22, 2006 11:47 PM (e)

Sir Toejam wrote:

the reason lenny calls you a liar, is that he knows well that your extremely limited understanding of the principles behind the referenced papers make them well beyond your ability to elucidate any substantive errors either in method or conclusion.

You might be interested in knowing I have a degree in biology. I spent two quarters in graduate school while I was applying to medical school. I’m currently taking a course in Quantum Mechanics at UCSB–one of the top-rated schools for physics in the U.S.

Whether you believe that or not does not detract in the least from the fact that it is all true. And if you don’t believe it, it’s just because you’re blinded by your prejudices. I can’t help that. You just like feeling smarter than other people. I suspect reality will catch up with you sooner or later. Ta Ta.

Comment #81646

Posted by Sir_Toejam on February 23, 2006 12:05 AM (e)

I spent two quarters in graduate school while I was applying to medical school. I’m currently taking a course in Quantum Mechanics at UCSB—one of the top-rated schools for physics in the U.S.

UCSB was my undergrad alma matter; it’s actually better known for it’s robotics and engineering school than it’s physics department per sae, tho i majored in aquatic biology there myself.

I’ve seen plenty of remarkably inept pre-med students in my day. What makes you any different?

oh that’s right, you made it two whole quarters in grad school before you what… washed out? don’t bring this stuff up unless you want to explore it.

what relevance does taking a course in mechanics at UCSB have on why you are so clueless on questions of biology? why aren’t you taking ecological physiology, or behavioral ecology, both of which have far more relevance to the subject material at hand?

you haven’t shown us the slightest inkling you understand what the hell you are talking about, and taking quantum mechanics ain’t gonna help you.

next you’ll tell us that your single course in quantum mechanics allows you to refute the entire theory of quantum mechanics.

phht.

your ‘arguments’ are assine, your intractability stupendous, and your relevance non-existent.

get the picture yet?

Comment #81647

Posted by Sir_Toejam on February 23, 2006 12:09 AM (e)

blast, your starting to affect my mental states.

please replace it’s with its.

ack.

Comment #81650

Posted by Sir_Toejam on February 23, 2006 12:10 AM (e)

hmm, how many errors can i make in a single paragrah…

replace your with you’re…

Comment #81655

Posted by Anton Mates on February 23, 2006 1:04 AM (e)

Sir_Toejam wrote:

you haven’t shown us the slightest inkling you understand what the hell you are talking about, and taking quantum mechanics ain’t gonna help you.

Actually, a QM class or two could be quite helpful for analyzing ID arguments. You may get some experience performing probability calculations. And you should certainly come out understanding that the history of the universe is one long string of improbable events, and that pointing at them afterwards and going “Wow, that was really improbable, someone must have planned it that way” doesn’t get you anywhere.

Assuming Blast is actually taking such a class, I doubt that’s the lesson he’ll walk away with–but again I think that’s due to his disinterest in understanding the natural world, rather than some basic inability to do so. He can reason quite well when he feels like it.

Comment #81859

Posted by BlastfromthePast on February 23, 2006 6:36 PM (e)

Anton Mates wrote:

Assuming Blast is actually taking such a class, I doubt that’s the lesson he’ll walk away with—but again I think that’s due to his disinterest in understanding the natural world, rather than some basic inability to do so.

Anton, it isn’t ‘disinterest’, or I wouldn’t be commenting here. I very much am interested in “understanding the natural world”, and I don’t think that can be done using neo-Darwinism. It’s mildly helpful; and disturbingly inadequate. When you’ve “walked through the Looking Glass”, as I have done with Darwinism, things look radically different. PTers can’t seem to handle the fact that someone can be reasonable and still doubt Darwin; so they resort to invective. I don’t think onlookers would consider that very flattering to the Darwinian cause.

Anyways, I have enjoyed your ability to be both civil and at the same time critical of an argument (…and paper: I’m almost finished reading the 1998 Borass article; I got it through the UCSB library system.)

Sir Toejam wrote:

UCSB was my undergrad alma matter; it’s actually better known for it’s robotics and engineering school than it’s physics department per sae, tho i majored in aquatic biology there myself.

It’s rated 8th to 9th in the United States after such schools as MIT, Cal-Tech, Harvard, Princeton, Stanford, Berkeley, UCLA–not bad company.

Sir Toejam wrote:

oh that’s right, you made it two whole quarters in grad school before you what… washed out? don’t bring this stuff up unless you want to explore it.

I don’t mind exploring. I dropped out when the professor I was doing lab work for asked me to falsify data for the grant application he was about to make. The only reason I was in graduate school was so that I could apply to medical school. And I entered during the Winter Quarter. Your ‘blindness’ seems to be acting up again.

Sir Toejam wrote:

why aren’t you taking ecological physiology, or behavioral ecology, both of which have far more relevance to the subject material at hand?

Why would I want to learn something that is, IMO, completely wrong? I pick up what I need to know as I go along.

Comment #81867

Posted by Sir_Toejam on February 23, 2006 7:05 PM (e)

Why would I want to learn something that is, IMO, completely wrong? I pick up what I need to know as I go along.

Oh, I don’t know, because you’re basing your opinion on crap rather than actual science?

why do you want to take a course on quantum mechanics then? surely you could just go on the internet and get all the relevant idiotic critiques available in ten minutes.

why don’t you post a link back to that discussion about front-loading and snake toxins we had Blast, if you want to submit the lurkers to your “informed opinion” on the matter?

You want us to take you seriously, but you won’t actually put any time into studying the relevant materials.

can’t you see how assinine that is??

… and you talk about OUR prejudices…

sheesh.

Comment #81869

Posted by Sir_Toejam on February 23, 2006 7:13 PM (e)

remember that word, blast…

projection.

when you accuse US of being biased, when most of us who criticize your front loading crap have ALREADY studied the relevant literature for years, that’s called projection.

any wonder why you piss so many of us off?

90% of your “arguments” essentially stem from projection on your part.

it gets tiresome to keep correcting you all the time.

not that you care, but i guess Anton does.

Comment #81875

Posted by Sir_Toejam on February 23, 2006 7:32 PM (e)

When you’ve “walked through the Looking Glass”, as I have done with Darwinism, things look radically different.

yeah, i hear regular doses of LSD can do that for ya.

what’s “Darwinism” again there, Blast? I’ve studied behavioral ecology and evolutionary biology for over 20 years and the only times I EVER hear this term is from the mouths of those who haven’t a clue what evolutionary biology is.

Please do define it for us, and then, by example, show how any of us here actually fits what a “Darwinist” is.

Yes, in case you hadn’t figured it out, I’m inviting you to do exactly what comes out of the use of your term: set up a strawman and tear it down for us.

always entertaining, if a bit droll.

PTers can’t seem to handle the fact that someone can be reasonable and still doubt Darwin; so they resort to invective.

wrong. all of us here have OVER AND OVER again, asked those who present what they think to be “contrarian” theories to TE to “put up or shut up”, essentially, come up with a testable hypothesis, go out and do the work to test it, get it published, and then we’ll talk.

instead, we find IDiots like yourself presenting concepts with no evidence in support, or even trying to rewrite the definition of science itself to make your crap “fit” like a round peg into a square hole.

you say you want to understand the natural world? bullshit. if you did, you would go out an try to test your front-loading concepts (not that you can even actually construct a testable hypothesis out of front-laoding, or ID to begin with).

no, you’d rather take quantum mechanics than learn how to potentially test your idea against the ones that have already been tested, found supporting evidence, and published regarding species variation.

Just like GoP, you would try to tear down 150 years of qualified experiments in the published literature, without even taking the time to understand how you might go about actually constructing real world experiments to test alternative theories.

no, you aren’t interesting in the NATURAL world, Blast, only your religious worldview.

I could personally care less if any lurkers think my treatment of you harsh, I will express my displeasure any time i get the chance, because your approach to the debate, a clear and proud declaration of the argument from ignorance, needs to be stamped out, hard, whenever it appears.

and..

you’re still a buffoon.

Comment #81876

Posted by Sir_Toejam on February 23, 2006 7:35 PM (e)

interesting=>interested.

Comment #81877

Posted by Sir_Toejam on February 23, 2006 7:41 PM (e)

Actually, a QM class or two could be quite helpful for analyzing ID arguments. You may get some experience performing probability calculations

irrelevant to the study of TE tho; as were Dembski’s arguments to begin with.

He can reason quite well when he feels like it.

It’s just that it’s so bloody rare that he “wants” to.

Comment #81910

Posted by Anton Mates on February 24, 2006 12:04 AM (e)

BlastfromthePast wrote:

Anton, it isn’t ‘disinterest’, or I wouldn’t be commenting here. I very much am interested in “understanding the natural world”, and I don’t think that can be done using neo-Darwinism. It’s mildly helpful; and disturbingly inadequate. When you’ve “walked through the Looking Glass”, as I have done with Darwinism, things look radically different. PTers can’t seem to handle the fact that someone can be reasonable and still doubt Darwin; so they resort to invective. I don’t think onlookers would consider that very flattering to the Darwinian cause.

I wish I could believe you. Unfortunately, I’ve seen you repeatedly make arguments which have flaws I know you’re quite capable of recognizing–as with the dice-rolling analogy above, for instance.

Why would I want to learn something that is, IMO, completely wrong? I pick up what I need to know as I go along.

Plenty of us have read work by, say, Behe or Dembski. If you don’t learn the material, how do you know it’s wrong? This thread was a good example of that…attempting to refute a paper you haven’t read yet is rarely fruitful!

Comment #81991

Posted by BlastfromthePast on February 24, 2006 10:26 AM (e)

Anton Mates wrote:

I wish I could believe you. Unfortunately, I’ve seen you repeatedly make arguments which have flaws I know you’re quite capable of recognizing—as with the dice-rolling analogy above, for instance.

What are you talking about? Where do you see the flaw?

Anton Mates wrote:

Plenty of us have read work by, say, Behe or Dembski. If you don’t learn the material, how do you know it’s wrong? This thread was a good example of that…attempting to refute a paper you haven’t read yet is rarely fruitful!

I didn’t have access to the paper. I’ve now read the entire paper and am quite sure that what we see is ‘induction’, despite the author’s pleading. The only way to be sure, is to run an experiment. And Borass is the only one to run it. But, of course, he won’t, because he’s quite satisfied that he’s proven that predation is an active selective force bringing about multicellularity via Darwinian mechanisms. This only affirms his ‘faith’ in the theory and wins him plaudits. So what’s his motivation for really getting to the bottom of it.

As to ‘learning’ about this stuff, what makes you think I haven’t read a lot of books? I’ve looked into the proposed mechanisms of evolution and they just don’t make sense: they’re either highly improbable, or inadequate from an ‘information needing to be generated’ point of view. Recombination doesn’t ‘invent’ new information. To have a new phyla/class of organisms, new information is needed. And, don’t forget, it’s from years ago, but I have a degree in biology. I’ve taken Chordate Morphology, Genetics, Developmental Biology, Cell Biology courses, etc. Michael Denton is a professional biologist, and he’s written one of the most influential books criticizing Darwinism. Why don’t you read that one?

As a mathematician, I don’t see how you can think Darwinism works. Why don’t you get and read Fred Hoyle’s book, “The Mathematics of Evolution”. See what he has to say there, and then make up your mind.

Comment #82050

Posted by Anton Mates on February 24, 2006 2:19 PM (e)

BlastfromthePast wrote:

What are you talking about? Where do you see the flaw?

Both Pim and I discussed the problems with your analogy upthread.

I didn’t have access to the paper. I’ve now read the entire paper and am quite sure that what we see is ‘induction’, despite the author’s pleading.

I’m sure that you’re sure. You’re welcome now to return to the problems pointed out with your hypothesis upthread. Such as the incredible ad hoc complexity an induction mechanism would have to involve in order to account for all the phenomena in this study, and the absence of evidence against the much simpler and independently confirmed mutation & selection mechanism, and the fact that the induction mechanism would have to fail half the time to account for all the instances when multicellularity didn’t occur.

The only way to be sure, is to run an experiment. And Borass is the only one to run it.

Um, no. Anyone is free to run any experiments they like to test any theories they like.

Speaking of which, Burkert, Hyenstrand Drakare and Blomqvist published “Effects of the mixotrophic flagellate Ochromonas sp. on colony formation in Microcystis aeruginosa” in Aquatic Ecology 35:1, 2001. (So a different prey species, a cyanobacterium, but the same predator.) They tried mixing Ochromonas and Microcystis directly, as well as two means of exposing Microcystis to potential chemical inducers from Ochromonas (growing them on either side of a dialysis membrane, and adding filtered Ochromonas culture to the Microcystis.)

What do you suppose they found? The Microcystis developed aggregates in only one case–when the dialysis membrane accidentally ruptured and the Ochromonas was allowed to prey directly on the Microcystis. In their other experiment involving direct predation, and in both of their experiments looking for chemical cues, there was no aggregation.

If you still want to argue chemical induction, that’s great–we’re well into “test it yourself” territory now, though.

But, of course, he won’t, because he’s quite satisfied that he’s proven that predation is an active selective force bringing about multicellularity via Darwinian mechanisms. This only affirms his ‘faith’ in the theory and wins him plaudits. So what’s his motivation for really getting to the bottom of it.

Gosh, somehow other researchers–such as Hessen and Van Donk, cited in this very paper–managed to overcome this vicious Darwinist peer pressure and publish papers on instances of development of multicellularity which were not due to mutation & selection. Even stranger, this didn’t sabotage their careers and in fact they’re both full professors now.

But of course those were real scientists, dedicated to truth, whereas Boraas was only out to get fame and fortune and was terrified of bucking mainstream orthodoxy in any fashion. Because he’s not just greedy and ambitious, he’s stupid too and therefore has no idea that overturning established theories is how you get fame and fortune in science. Poor dumb guy.

As to ‘learning’ about this stuff, what makes you think I haven’t read a lot of books? I’ve looked into the proposed mechanisms of evolution and they just don’t make sense: they’re either highly improbable, or inadequate from an ‘information needing to be generated’ point of view. Recombination doesn’t ‘invent’ new information. To have a new phyla/class of organisms, new information is needed.

Again, if you’re really taking a quantum class, and doing reasonably well in it, you should be seeing the holes in this improbability argument. Everything is here because of a series of improbable events. As for “an ‘information needing to be generated’ point of view,” yeesh…sorry, but that’s been shown as a red herring over and over and over again. Have you stopped by the math department and asked any of the professors there what they think of that argument?

And, don’t forget, it’s from years ago, but I have a degree in biology. I’ve taken Chordate Morphology, Genetics, Developmental Biology, Cell Biology courses, etc.

That’s great. But I was responding to your claim that you don’t need to take classes on theories you think are wrong.

Michael Denton is a professional biologist, and he’s written one of the most influential books criticizing Darwinism. Why don’t you read that one?

Will do. Just pulled it out of the library.

As a mathematician, I don’t see how you can think Darwinism works.

Er…perhaps there’s a lesson to be learned there? If the mathematical community’s completely unimpressed by attempted mathematical refutations of evolutionary theory–if the guy who developed the No Free Lunch theorems Dembski tried to use against evolution took the trouble to say, “No, they’re inapplicable here and his use of them is shoddy”–if even I can find undergrad-class errors in his work–then maybe that shows there isn’t a good math-based argument against “Darwinism” after all?

I mean, it’s not like the average mathematician cares one way or the other about evolutionary theory (although I do). They have no interest whatsoever in preserving Darwin’s reputation or keeping biologists happy. Quite the contrary, if they could demonstrate the necessary failure of evolutionary algorithms they’d trumpet it to the four winds…not only other mathematicians but all the comp sci guys would love to know about that.

Why don’t you get and read Fred Hoyle’s book, “The Mathematics of Evolution”. See what he has to say there, and then make up your mind.

Sure, I’ll take a look at it. It’s not in this campus library, unfortunately, but I put in a request to ship it in from one of the other campuses.

Comment #82123

Posted by BlastfromthePast on February 24, 2006 11:55 PM (e)

BlastfromthePast wrote:

That’s not how I see it. There are three substances A, B, and C. A is produced by the unicells in an on-going manner. B is produced either by the dying algae directly, or in conjunction with the predator. Substance B then in turn causes substance C to be produced, which is the ‘trigger’ for the colonial form of the algae…..

I don’t see the problem if you think of this in terms of an ‘on/off’ switch. Unicell Chlorella prefers the unicellular form (as you tell it, the paper says that the unicellular form is more efficient in absorbing light and nutrients than the colonial form) and normally is producing substance A. Along comes the predator, substance B is produced, and the Chlorella ‘switch over’ to producing substance C. It’s not the case that the Chlorella are producing both A and C on a proportional basis, rather, when B is high enough (think in terms of the activation energy needed for chemical reactions) the Chlorella starts producing C alone. Now you have to think in terms of an ‘activation energy’ again for the Chlorella to go back to producing substance A again. So, being that there is a switch mechanism, once the colonial form is established, AND, in a ‘monospecific’ environment, it will keep on being colonial. Only in the presence of very high A will the colonial form ‘switch back’ to producing unicellular forms and substance A (rather than C). [There is a presumption that the Chlorella is more sensitive to the A signal than the C signal, so that where both are present in relatively equal amounts, the A signal will prevail] Where does the ‘very high’ A come from? It comes from some nearby area where the presence of the predator is low, or almost completely absent; and this ‘substance A producing area’ then spreads until it comes into contact with the colonial form, at which point, the Chlorella go back to the unicellular form. So then, likewise, in the presence of a predator, high concentrations of B are produced, the Chlorella ‘switch over’, and at a high enough concentration of B, spread over a large enough area (encompassing an exceedingly large number of Chlorella),the colonial form begins to take hold, and then this ‘substance C producing area’ begins to spread.

Anton Mates wrote:

Chemostats are constantly stirred, and Chlorella has to be aerated. There aren’t going to be slowly spreading areas of “high concentration.” Moreover, colonial Chlorella is maintained even in cultures that have low predator densities and some of the unicellular morph.

Somehow I didn’t see this post earlier.

As to your comment about stirring, in what I had to say, I was talking about the real world, not about the chemostats. In the chemostat, the scenario I proposed applies. In stage one, there is high A; in the second stage there is high C (predators+unicells=production of B, which in turn stimulates production of C), and low A (the predators are eating up the A producers). I don’t think your objections hold.

Anton Mates wrote:

Blast: In an earlier post wrote:

“It’s clear from the article that the reason for the colonial form to ‘wash out’ was the lack of light. In a low-light situation, the colonial form might not survive well at all. In fact, I wouldn’t be surprised if the colonial form didn’t arise even in the presence of the predator unless there was a high level of light available. So you don’t have a situation in the two-stage chemostat where a ‘substance A producing area’ could spread—whatever amount of A that was being produced by the unicells in the first stage was diluted by the C being produced by those surviving unicells in the presence of the predator in stage two.”

Wait, what? The situation we have is that the colonials arise in the second stage when the lights are on, and disappear (and are replaced by single cells which are known to be descendants of the first stage, because of their smaller size) when the lights are off. Are you saying that when the colonials disappear, that is evolution in this particular case?

I don’t understand what you mean by the last sentence. I was merely saying that it’s quite clear from the article that the colonial form ‘dies off’ in a ‘darkened’ chemostat (i.e., the second stage)

There is nothing that says some other sort of signaling can’t take place whereby the colonial Chlorella, sensing the environment that they’re in, settle on an appropriate cell-number.

Anton Mates wrote:

Good God. More hypothetical signals? Substances A,B and C plus whatever internal chemical arrays lead to switchover hysteresis (your “activation energies”) plus light-sensitivity plus some other chemical network whereby the Chlorella all get together and agree that, yes, because this particular flagellate can’t eat eight cells, they should all switch over to that?

It’s entirely possible that there is some kind of genetic algorithm built into the alga that monitors its efficiency relative to predator success and the amount of nutrients that are being absorbed, etc. Remember it’s called ‘intellgent design’; not ‘intelligent roulette wheel spinning’. There’s plenty of room for purposeful structures in the genome.

Anton Mates wrote:

Blast wrote in an earlier post:
“Nonetheless, I would think there would be some preferred sizes—just from the physics of the whole thing.”

What they found, repeatedly, is that there aren’t preferred sizes until several generations have passed. Initially there’s a ton of colony sizes. After a while, there’s only one or two. And the physics doesn’t change in that time period.

By physics, I was referring to such things as volume/surface area ratio and its effect on photosynthesis efficiency and absorption efficiency.

Anton Mates wrote:

BlastfromthePast wrote:

But to think that RM+NS will operate in a repeatable fashion (this phenomena reappears 70% of the time) means that the right mutation has to occur at the right place, at the right time, 70% of the time.

Nope, that’s neither what the data suggests nor what an evolutionary explanation requires. 70% of the cultures ended up mostly eight-celled—that simply means that one of the right mutations or combos of mutations has to occur in one of the millions of cells in 70% of your cultures. And as Pim points out, “the right time” just means “any time in the history of the culture before now.” Of course a colonial morph in the culture before the flagellate was introduced might well wash out, but the eight-celled forms usually didn’t appear until anywhere from forty to eighty generations after the introduction.

Given typical measured mutation rates, that implies literally millions of random mutations in the coding regions of the Chlorella genome—even if we ignore mutations that occurred before the flagellate was introduced. And just one of them needs to produce an 8-celled form by some not-horribly-debilitating mechanism.

Furthermore, the 8-cell form need not arise directly; almost any colonial morph is initially selected for, since any colony with more than 4 cells doesn’t get eaten. So if a 16-cell morph happens to arise first, it’s likely to stick around and possibly evolve to an 8-celled form a few generations later.

This is where ‘Alice in Wonderland’ sets in. I’m going to respond in a “let’s step back and look at the ‘big picture’” mode:

(1) According to what you and Pim seem to understand as mutation and selection, it is safe to say that what was there at the beginning of the experiment, was there at the end of the experiment. Nothing changed except for population density.

And this is “mutation” and “selection”? What mutated? According to your logic there was at least ‘one’ (or to sort of paraphrase you, ‘one in a million’) Chlorella form that was, let us say, ‘ancestral’ to the colonial form. And then, because of the so-called “selective effect” brought about by the presence of the predator, this form was “favored”, and eventually displaced the unicellular form. Well, what was preventing the colonial form from multiplying into a larger percent of the total population before the predator appeared? Well, you’ll say, the unicell form is more ‘fit’ than the colonial form. Okay, that’s reasonable. But why is the ratio a million to one in an ambient where nutrient and light were available (stage one chemostat)? It would be nice to have the data concerning how, and under what conditions, and to what degree, the unicell was more ‘competitive’ than the colonial–but, the data was not published. How interesting.

So, big picture, according to your view, the so-called ‘mutation’ is already there, but not multiplying. Then the predator comes along, and it multiplies exponentially. Sounds like a triggering mechanism is in place.

(2) There are other zooplankton that convert to multicellular forms. Experimenters have determined that a ‘trigger’ chemical–an inducer–is released that brings about the multicellular form. That’s the rule. Chlorella is the exception. I think it safer to look for some kind of chemical induction than to look for—–well, what do we call it? I can’t call it ‘evolution’, or ‘random mutation’, so what do I call it? It’s not ‘evolution’, since what was there at the end, was there at the beginning; and it’s not ‘random mutation’ because, sorry, you can’t have so-called mutations hit on the same defense mechanism 70% of the time and then call that ‘random.’ So, it’s some kind of conversion mechanism. That sounds like the best way to describe it.

(3) The colonial form bred true for two years. And we’re told that the unicell form is more competitive, more ‘fit’, than the colonial form. Now pay close attention here, why did it take only 10-20 generations to ‘mutate’ to the more ‘fit’ colonial form when the predator was present, but after two years there’s no sign whatsoever of a ‘mutation’ to convert the colonial form to the more ‘fit’ unicell form in an environment where the predator is no longer present?

What do they say: What’s good for the goose, is good for the gander? (You mean there wasn’t even ONE unicell form among the colonial that could be ‘selected’ for?)

Comment #82170

Posted by Anton Mates on February 25, 2006 2:57 PM (e)

BlastfromthePast wrote:

As to your comment about stirring, in what I had to say, I was talking about the real world, not about the chemostats. In the chemostat, the scenario I proposed applies. In stage one, there is high A; in the second stage there is high C (predators+unicells=production of B, which in turn stimulates production of C), and low A (the predators are eating up the A producers). I don’t think your objections hold.

OK, but these experiments took place in chemostats, so how the mechanism works in the “real world” isn’t very relevant. You still need to explain why, with even low densities of predators (therefore low B, right?) and large numbers of the unicellular morph (therefore high A), the colonies still arise and persist. Remember, in the two-stage chemostat there’s a ton of unicellular Chlorella in the first stage, and any substances they’re pumping out will get carried along with them into the second stage.

Wait, what? The situation we have is that the colonials arise in the second stage when the lights are on, and disappear (and are replaced by single cells which are known to be descendants of the first stage, because of their smaller size) when the lights are off. Are you saying that when the colonials disappear, that is evolution in this particular case?

I don’t understand what you mean by the last sentence. I was merely saying that it’s quite clear from the article that the colonial form ‘dies off’ in a ‘darkened’ chemostat (i.e., the second stage)

And that at least is evolution, yes? Since as I explained it is extremely unlikely that the colonies literally die, being mixotrophic. They simply don’t do well enough to compensate for population loss due to medium cycling and competition with the unicellular form.

Plus, we know that the unicellular form continues to metabolize and grow in the darkened stage–it just doesn’t go colonial, in spite of the fact that it’s getting munched by the predator just as it was when the lights were on. That means you have to add even more signaling mechanisms to your already Einstein-brilliant Chlorella, to account for this light-sensitivity.

It’s entirely possible that there is some kind of genetic algorithm built into the alga that monitors its efficiency relative to predator success and the amount of nutrients that are being absorbed, etc. Remember it’s called ‘intellgent design’; not ‘intelligent roulette wheel spinning’. There’s plenty of room for purposeful structures in the genome.

Sure, and there’s room for part of the genome to contain the code for Tetris. But you need evidence for your ten or so inducing/signalling substances and the long-distance sensor arrays which somehow scan the rest of the culture to see how the colonies of various sizes are doing.

By physics, I was referring to such things as volume/surface area ratio and its effect on photosynthesis efficiency and absorption efficiency.

OK, but again, the rules governing those effects didn’t change during the experiment–the eight-celled form always had an advantage over the larger forms in terms of volume/area and nutrient uptake. So the initial explosion of variously-sized colonies, followed by the dominance of the eight-celled form, must have occurred for some other reason. Like, say, mutation followed by selection…

(1) According to what you and Pim seem to understand as mutation and selection, it is safe to say that what was there at the beginning of the experiment, was there at the end of the experiment. Nothing changed except for population density.

No, that’s wrong. What Pim was saying, and what I echoed, is that the mutation could have been there prior to the flagellate introduction. The mutation was just as likely to occur then as later–perhaps more likely because the Chlorella population was larger. On the flip side, a mutant which arose long before the flagellate was around is likely to have died out before the introduction of the latter. So there’s no compelling reason to think that the mutation which finally won out must have occurred either before or after the introduction…both are possibilities.

And this is “mutation” and “selection”? What mutated? According to your logic there was at least ‘one’ (or to sort of paraphrase you, ‘one in a million’) Chlorella form that was, let us say, ‘ancestral’ to the colonial form. And then, because of the so-called “selective effect” brought about by the presence of the predator, this form was “favored”, and eventually displaced the unicellular form. Well, what was preventing the colonial form from multiplying into a larger percent of the total population before the predator appeared? Well, you’ll say, the unicell form is more ‘fit’ than the colonial form. Okay, that’s reasonable. But why is the ratio a million to one in an ambient where nutrient and light were available (stage one chemostat)?

Huh? What ratio? Do you mean relative fitness? And where did you get “a million to one” from? Neither morph has to be a million times fitter than the other in the current environment to displace it…it only has to be 1.000000001 times fitter!

It would be nice to have the data concerning how, and under what conditions, and to what degree, the unicell was more ‘competitive’ than the colonial—but, the data was not published. How interesting.

Sure it was. In an illuminated environment, when the flagellate is present at all, no matter how few its numbers, the colonial morph is more competitive until it almost completely dominates the culture, at which point a small amount of the unicellular morph can compete. When the lights go out, the unicellular morph is much fitter no matter what the predation situation is. And when the lights stay on but the flagellate’s removed, the unicellular morph is slightly fitter and “slowly” outcompetes the colonial morph. That’s more than enough data to publish on.

By the way, the above data provides a good example of the predictive power of evolutionary theory. The colonial morph, as the researchers observed directly, is more resistant to predation, while the unicellular morph is predictably better at nutrient uptake for geometric reasons. Now the benefits of superior nutrient uptake–in a well-mixed, well-cycled medium–should remain more or less constant regardless of the population counts of the various morphs and species. But the benefits of predation resistance are density-dependent; as the population of the colonial morph increases, the predators become fewer and less successful, and predation pressure is therefore weaker for both morphs. Therefore, it can be predicted that even under high predation pressures, the unicellular morph population will stabilize short of total extinction, whereas if predation pressure’s absent, nothing stops the colonial morph from washing out completely.

Which is, you’ll note, precisely what happens.

So, big picture, according to your view, the so-called ‘mutation’ is already there, but not multiplying. Then the predator comes along, and it multiplies exponentially. Sounds like a triggering mechanism is in place.

When you say things like that, it makes it very hard to believe you took several biology courses. Any organism multiplies exponentially if there’s room for it to do so–did you really not know that? And of course there is room in this case–the colonial morph becomes dominant immediately after a population crash due to predation, which leaves the culture wide open to repopulation.

(2) There are other zooplankton that convert to multicellular forms. Experimenters have determined that a ‘trigger’ chemical—an inducer—is released that brings about the multicellular form. That’s the rule. Chlorella is the exception. I think it safer to look for some kind of chemical induction than to look for——-well, what do we call it?

Chlorella isn’t zooplankton. Again, if you want us to believe you took bio courses…

And yeah, the conservative a priori guess would be that this was induction. That’s why Boraas took the time to rule that out.

I can’t call it ‘evolution’, or ‘random mutation’, so what do I call it? It’s not ‘evolution’, since what was there at the end, was there at the beginning; and it’s not ‘random mutation’ because, sorry, you can’t have so-called mutations hit on the same defense mechanism 70% of the time and then call that ‘random.’ So, it’s some kind of conversion mechanism. That sounds like the best way to describe it.

See, this is exactly what I was talking about–you demonstrate so clearly your disinterest in having an honest discussion.

1) There’s no reason to think the colonial mutants that became successful were present from the beginning.

2) Even if they were, change in the frequencies of pre-existing alleles is still evolution. You know this. You’d call it “micro-evolution,” and it certainly wouldn’t be as interesting a case as what did happen here, but it would be evolution. Even IDers and YECs would agree on that.

3) “So-called mutations” did not hit on the same defense mechanism 70% of the time–no one’s suggesting they did except you. And you know this too, because you paraphrased me as saying “1 in a million” previously. You’re simply choosing to ignore that and return to your “70% of cultures featured 8-celled forms –> 70% of mutations produced 8-celled forms” claim because–well, otherwise you’d have to admit error, I suppose.

Which isn’t really unexpected, given how you danced around the issue of the “kind” of Helacyton gartleri in an earlier thread, but is rather depressing.

(3) The colonial form bred true for two years. And we’re told that the unicell form is more competitive, more ‘fit’, than the colonial form. Now pay close attention here, why did it take only 10-20 generations to ‘mutate’ to the more ‘fit’ colonial form when the predator was present, but after two years there’s no sign whatsoever of a ‘mutation’ to convert the colonial form to the more ‘fit’ unicell form in an environment where the predator is no longer present?

What do they say: What’s good for the goose, is good for the gander? (You mean there wasn’t even ONE unicell form among the colonial that could be ‘selected’ for?)

First of all, your numbers are off–did you really read the paper? The colonial morph bred true for “several months,” not two years. It was maintained for two years in the presence of the flagellate, but that wasn’t testing for true breeding–there could have been a small unicellular population kept down by the predator. On top of that, the average time-to-appearance of the colonial morphs was not 10-20 generations–that was the time it took for the eight-celled morph to dominate the culture after the appearance of colonies. Rather, “colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates,” (with an upper bound, from the abstract, of “less than 100 generations.”). Factor in the 30% of cultures where colonial morphs failed to appear at all in the timeframe of the experiment, and the average time-to-appearance must have been greater than 20 generations. And of course the time-to-appearance is only a lower bound on the time it takes for the mutation to actually occur, since it could have occurred prior to flagellate introduction.

So, to sum up, we’re talking something like an average of a couple of weeks, maybe more, for observed unicellular-to-colonial mutations, vs. more than “several months” for observed mutations in the opposite direction. Not, as you’re suggesting, a week or so vs. two years.

Now it’s definitely the case that Chlorella went more “readily” from a unicellular to a viable multicellular form than vice versa. Which is interesting, certainly. But does it conflict with a mutation & selection scenario? Not at all. There’s absolutely no reason why the two transitions should average the same amount of time to occur.

Think about it. What factors affect the likelihood of a given phenotypic change due to mutation? Well, among other things:
1) the size of the population (bigger population = larger mutation rate),
2) the number of possible mutations that could produce said phenotypic change, and
3) the location of those mutations in more or less easily damaged parts of the genome.

Now 3) we can probably rule out here, since wherever a mutation could occur to induce multicellularity, presumably a second mutation at the same location could reverse it. But 1) is definitely a factor: we know that the colonial morph is outcompeted by the unicellular morph in the absence of predation, so it must have a lower reproductive rate–therefore its steady-state population in a given chemostat will be smaller. Moreover the colonial monocultures were recently grown, from a few Chlorella that must have been hand-selected to make sure they were colonial. So the present and past colonial population sizes were necessarily smaller than the same for the unicellular morph, therefore by 1) mutations should be less common.

As for 2), well, we don’t know much of anything about the exact mutations involved here. But there are many scenarios that would make unicellular-to-multicellular mutations more numerous than the reverse. For instance, we know that one of the mechanisms inducing colonialism here is incomplete breakdown of the mother cell wall after division. Suppose Chlorella’s got a gene which codes for an enzyme which breaks down that wall? Many mutations could inactivate that gene or severely disrupt enzyme function, say by frameshift; a much smaller number could reverse that effect. (IDers should be plenty familiar with that argument! “Mutations are always harmful,” right?)

Of course I just made that possibility up. But that’s the point–many possibilities exist for the precise mechanism producing the mutant colonial phenotype, and unless you can somehow rule most of them out, you can’t make any claims for how fast the colonial morph “should” be able to produce a viable unicellular mutant.

So…while it’s certainly worth looking into as to why the colonies didn’t mutate to unicellular morphs as rapidly as vice versa, it has no bearing on whether a mutation/selection model actually works here.

Comment #82422

Posted by BlastfromthePast on February 27, 2006 6:37 AM (e)

Anton: I’m just going to intersperse my remarks again.

“BlastfromthePast wrote:
As to your comment about stirring, in what I had to say, I was talking about the real world, not about the chemostats. In the chemostat, the scenario I proposed applies. In stage one, there is high A; in the second stage there is high C (predators+unicells=production of B, which in turn stimulates production of C), and low A (the predators are eating up the A producers). I don’t think your objections hold.”

Anton Mates wrote:
OK, but these experiments took place in chemostats, so how the mechanism works in the “real world” isn’t very relevant.

[[[[You mean we should just block out what nature might be telling us about the feasibility of this proposed scenario?]]]]]]

You still need to explain why, with even low densities of predators (therefore low B, right?) and large numbers of the unicellular morph (therefore high A), the colonies still arise and persist. Remember, in the two-stage chemostat there’s a ton of unicellular Chlorella in the first stage, and any substances they’re pumping out will get carried along with them into the second stage.

[[[Here’s a quote from the paper: ”Flagellates and Chlorella unicells in this steady state had population densities reduced to about 0.1% of their maximum numbers during the transient phases.” So “A” did not outnumber “B”.]]]]

BlastfromthePast wrote:

Anton Mates wrote:

“Wait, what? The situation we have is that the colonials arise in the second stage when the lights are on, and disappear (and are replaced by single cells which are known to be descendants of the first stage, because of their smaller size) when the lights are off. Are you saying that when the colonials disappear, that is evolution in this particular case?”

“I don’t understand what you mean by the last sentence. I was merely saying that it’s quite clear from the article that the colonial form ‘dies off’ in a ‘darkened’ chemostat (i.e., the second stage)”

Anton responds: “And that at least is evolution, yes? Since as I explained it is extremely unlikely that the colonies literally die, being mixotrophic. They simply don’t do well enough to compensate for population loss due to medium cycling and competition with the unicellular form.
Plus, we know that the unicellular form continues to metabolize and grow in the darkened stage—it just doesn’t go colonial, in spite of the fact that it’s getting munched by the predator just as it was when the lights were on. That means you have to add even more signaling mechanisms to your already Einstein-brilliant Chlorella, to account for this light-sensitivity.”

[[[[[[[[You make a good point, Anton. I think you’ve analyzed that portion of the experiment much better than I. But I would quibble with you quite heartily over the term ‘evolution’—again, what ‘new’ form has been brought about; it would seem we just have ‘unicell’ Chlorella (same as before) that are kept inside the mother cell wall. This now leads to a response to the supposed need for added ‘signaling mechanisms.”

It would be quite reasonable—certainly plausible—that the ‘mother cell wall’ would reduce the amount of light that the ‘unicell’ (more or less) Chlorella would receive. So, in a low light situation, the ‘colonial’ form, lacking the ‘energy’ needed for cell division, just couldn’t keep up with the true unicell Chlorella (thus leading to ‘washout’), irrespective of whatever signaling was taking place.]]]]]]

BlastfthePast wrote: “It’s entirely possible that there is some kind of genetic algorithm built into the alga that monitors its efficiency relative to predator success and the amount of nutrients that are being absorbed, etc. Remember it’s called ‘intelligent design’; not ‘intelligent roulette wheel spinning’. There’s plenty of room for purposeful structures in the genome.”

Anton Mates responded: “Sure, and there’s room for part of the genome to contain the code for Tetris. But you need evidence for your ten or so inducing/signaling substances and the long-distance sensor arrays which somehow scan the rest of the culture to see how the colonies of various sizes are doing.”

[[[[[From some other reading, it appears that a likely candidate for inducer “B” is simply something that spills out of the unicell form when it’s eaten by the flagellate. Thus, even “B” is not anything that has to be produced via an exceptional route. And as I stated above, the light-reducing effect of the mother cell wall is enough to explain the ‘washing out’ of the colonial form. So, we’re left with really one new chemical inducer, “C”, which likely affects the adhesive properties of daughter cells to the mother cell wall. Very simple, really. But ID certainly doesn’t put limits on the information-processing capacity of genetic life.]]]]]]]]

BlastfrthePast wrote: “By physics, I was referring to such things as volume/surface area ratio and its effect on photosynthesis efficiency and absorption efficiency.”

Anton responded: “OK, but again, the rules governing those effects didn’t change during the experiment—the eight-celled form always had an advantage over the larger forms in terms of volume/area and nutrient uptake. So the initial explosion of variously-sized colonies, followed by the dominance of the eight-celled form, must have occurred for some other reason. Like, say, mutation followed by selection…”

[[[[[Did I say the ‘rules of physics’, or simply ‘physics’. No, the ‘rules’ didn’t change; but the volume/surface area sure changed as the Chlorella went from unicell to 8-cell, to….100-cell forms. Are you making a concerted effort to misunderstand what I’m saying? As to “mutation followed by selection…”; well, if it’s ‘induction’, then it’s not ‘mutation’. So aren’t you jumping the gun here?]]]]]]]

Blast wrote: “(1) According to what you and Pim seem to understand as mutation and selection, it is safe to say that what was there at the beginning of the experiment, was there at the end of the experiment. Nothing changed except for population density.”

Anton responds: “No, that’s wrong. What Pim was saying, and what I echoed, is that the mutation could have been there prior to the flagellate introduction. The mutation was just as likely to occur then as later—perhaps more likely because the Chlorella population was larger. On the flip side, a mutant which arose long before the flagellate was around is likely to have died out before the introduction of the latter. So there’s no compelling reason to think that the mutation which finally won out must have occurred either before or after the introduction…both are possibilities.”

[[[[Here’s a quote from Pim’s post #80680: “You may misunderstand evolutionary theory here. Mutations do not happen because they are needed but rather mutations are present in the original stock and are selected for.” Does this sound like Pim was saying it “could have been there prior to the flagellate introduction”?]]]]]

Blast wrote: “And this is “mutation” and “selection”? What mutated? According to your logic there was at least ‘one’ (or to sort of paraphrase you, ‘one in a million’) Chlorella form that was, let us say, ‘ancestral’ to the colonial form. And then, because of the so-called “selective effect” brought about by the presence of the predator, this form was “favored”, and eventually displaced the unicellular form. Well, what was preventing the colonial form from multiplying into a larger percent of the total population before the predator appeared? Well, you’ll say, the unicell form is more ‘fit’ than the colonial form. Okay, that’s reasonable. But why is the ratio a million to one in an ambient where nutrient and light were available (stage one chemostat)?”

Anton responds: “Huh? What ratio? Do you mean relative fitness? And where did you get “a million to one” from?

[[[I’m afraid I got it from you. You threw out the number upthread somewhere.]]]]

Neither morph has to be a million times fitter than the other in the current environment to displace it…it only has to be 1.000000001 times fitter!”

[[[I’ll assume that the two ‘morphs’ of Chlorella, in stage one, compete for the Nitrogen. Otherwise, this wouldn’t be true.]]]]

Blast-Past wrote: “It would be nice to have the data concerning how, and under what conditions, and to what degree, the unicell was more ‘competitive’ than the colonial—but, the data was not published. How interesting.”

Anton responds: “Sure it was. In an illuminated environment, when the flagellate is present at all, no matter how few its numbers, the colonial morph is more competitive until it almost completely dominates the culture, at which point a small amount of the unicellular morph can compete. When the lights go out, the unicellular morph is much fitter no matter what the predation situation is. And when the lights stay on but the flagellate’s removed, the unicellular morph is slightly fitter and “slowly” outcompetes the colonial morph. That’s more than enough data to publish on.”

[[[[[Yes, but they wrote: “In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the light, the multicellular from was slowly displaced by unicells (data not shown).” p.160 Do you see my point now?]]]]]]

Anton continues: “By the way, the above data provides a good example of the predictive power of evolutionary theory. The colonial morph, as the researchers observed directly, is more resistant to predation, while the unicellular morph is predictably better at nutrient uptake for geometric reasons. Now the benefits of superior nutrient uptake—in a well-mixed, well-cycled medium—should remain more or less constant regardless of the population counts of the various morphs and species. But the benefits of predation resistance are density-dependent; as the population of the colonial morph increases, the predators become fewer and less successful, and predation pressure is therefore weaker for both morphs. Therefore, it can be predicted that even under high predation pressures, the unicellular morph population will stabilize short of total extinction, whereas if predation pressure’s absent, nothing stops the colonial morph from washing out completely.
Which is, you’ll note, precisely what happens.”

[[[[So that proves that the normal form of Chlorella outside of predation is the unicell. But, of course, we already knew that. ]]]]]

BlastfromthePast wrote: “So, big picture, according to your view, the so-called ‘mutation’ is already there, but not multiplying. Then the predator comes along, and it multiplies exponentially. Sounds like a triggering mechanism is in place.”

Anton responds: “When you say things like that, it makes it very hard to believe you took several biology courses. Any organism multiplies exponentially if there’s room for it to do so—did you really not know that? And of course there is room in this case—the colonial morph becomes dominant immediately after a population crash due to predation, which leaves the culture wide open to repopulation.

[[[[[Why do you focus in on the “exponential” part? And why do you even begin to suspect that I don’t know something as elementary as that? The point is that ‘according to your view’, what wouldn’t ‘grow’ before is now ‘growing’. So WHAT caused it to start ‘growing’? IOW, what ‘triggered’ the growth response? If the ‘unicell’ form has to only be 1.000000001 fitter than the ‘colonial’ form to outcompete it (your numbers), then why all of a sudden does it start to ‘outcompete’ the unicell form? Please explain. Remember that (1) ‘low’ unicell also results in ‘low’ predator, and (2) ‘low’ unicell means 0.1 % of its maximum density. Therefore, if the ‘mutant’ form exists, the ‘unicell’ has only declined in numbers by 10^3, whereas its fitness factor , relative to the colonial form (using your numbers) is 10^8. So the ‘colonial’ form should still be ‘outcompeted’–according to your logic.]]]]]]

Blast wrote: “(2) There are other zooplankton that convert to multicellular forms. Experimenters have determined that a ‘trigger’ chemical—an inducer—is released that brings about the multicellular form. That’s the rule. Chlorella is the exception. I think it safer to look for some kind of chemical induction than to look for——-well, what do we call it?”

Anton responds: “Chlorella isn’t zooplankton.

[[[[[But it’s closely related.]]]]]

Again, if you want us to believe you took bio courses…

[[[[[[Why this tendency to prejudge? If you’ll look at an earlier post, you’ll see that I called Chlorella an algae.]]]]

And yeah, the conservative a priori guess would be that this was induction. That’s why Boraas took the time to rule that out.

[[[[Has he, in fact, ruled it out? Here’s a quote: “Our results could be interpreted as evidence that the flagellates released a substance inducing colony formation in Chlorella, ……..We discount this alternative hypothesis, based on four observations……”p.159 He ‘discounted’ it; he didn’t ‘rule it out.’ This isn’t just semantics here.]]]]]]

Blast wrote: “I can’t call it ‘evolution’, or ‘random mutation’, so what do I call it? It’s not ‘evolution’, since what was there at the end, was there at the beginning; and it’s not ‘random mutation’ because, sorry, you can’t have so-called mutations hit on the same defense mechanism 70% of the time and then call that ‘random.’ So, it’s some kind of conversion mechanism. That sounds like the best way to describe it.”

Anton responds (attacks?): “See, this is exactly what I was talking about—you demonstrate so clearly your disinterest in having an honest discussion.
1) There’s no reason to think the colonial mutants that became successful were present from the beginning.

[[[[[Please refer to Pim’s quote in #80680]]]]]]]

2) Even if they were, change in the frequencies of pre-existing alleles is still evolution. You know this. You’d call it “micro-evolution,” and it certainly wouldn’t be as interesting a case as what did happen here, but it would be evolution.

[[[[Yes. It would be an ‘interesting case’, IF that’s what happens. But aren’t we arguing over exactly what did happen? Why jump the gun?]]]]]

Even IDers and YECs would agree on that.
3) “So-called mutations” did not hit on the same defense mechanism 70% of the time—no one’s suggesting they did except you. And you know this too, because you paraphrased me as saying “1 in a million” previously. You’re simply choosing to ignore that and return to your “70% of cultures featured 8-celled forms —> 70% of mutations produced 8-celled forms” claim because—well, otherwise you’d have to admit error, I suppose.

[[[[[ Please pay attention. Here’s a quote: ”After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.” (My emphasis) Please explain how the ‘solution’ to the ‘problem of a predator’ is solved in the same way each and every time the experiment is tried? This I’ve got to see.]]]]]]

Which isn’t really unexpected, given how you danced around the issue of the “kind” of Helacyton gartleri in an earlier thread, but is rather depressing.

[[[[We’re getting a little nasty here, aren’t we? Here’s an answer: a “kind” is a “paradigmatic form”. Okay? As if I really need to explain what it is. Shall I explain what a chair is also? I bet you know one when you see one.]]]]]]

Blast wrote: (3) The colonial form bred true for two years. And we’re told that the unicell form is more competitive, more ‘fit’, than the colonial form. Now pay close attention here, why did it take only 10-20 generations to ‘mutate’ to the more ‘fit’ colonial form when the predator was present, but after two years there’s no sign whatsoever of a ‘mutation’ to convert the colonial form to the more ‘fit’ unicell form in an environment where the predator is no longer present?
What do they say: What’s good for the goose, is good for the gander? (You mean there wasn’t even ONE unicell form among the colonial that could be ‘selected’ for?)”

Anton writes: “First of all, your numbers are off—did you really read the paper?

[[[[Must you always attack? Did you read the paper? Here’s a quote: ”…(w)hen the colonies are cultured in the absence of any source of an inducing substance, the colonies ‘breed true’.” p.159 I guess I didn’t read it. Here they seem to suggest that the ‘colonies’ keep this up indefinitely. ]]]]

“The colonial morph bred true for “several months,” not two years. It was maintained for two years in the presence of the flagellate, but that wasn’t testing for true breeding—there could have been a small unicellular population kept down by the predator.

[[[[Are you, by any chance, referring to this statement: p.159/160 “The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have been maintained for several months.” My reading of this is that the ‘several months’ refers only to the chemostats kept at steady states. You’re wrong here, and that affects the argument you construct below.]]]]]]]

On top of that, the average time-to-appearance of the colonial morphs was not 10-20 generations—that was the time it took for the eight-celled morph to dominate the culture after the appearance of colonies.

Rather, “colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates,”

[[[[I don’t see the difference between what you’re saying and the quote above that is taken from the paper: “After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph….p. 160 The ‘inoculation’ introduced the ‘presence’ of the phagotroph.]]]]]

(with an upper bound, from the abstract, of “less than 100 generations.”). Factor in the 30% of cultures where colonial morphs failed to appear at all in the timeframe of the experiment,

[[[[[[Please confer the quote from the paper that says ‘all’ replicates formed the 8-celled colonial form.]]]]]]

and the average time-to-appearance must have been greater than 20 generations. And of course the time-to-appearance is only a lower bound on the time it takes for the mutation to actually occur, since it could have occurred prior to flagellate introduction.
So, to sum up, we’re talking something like an average of a couple of weeks, maybe more, for observed unicellular-to-colonial mutations, vs. more than “several months” for observed mutations in the opposite direction. Not, as you’re suggesting, a week or so vs. two years.
Now it’s definitely the case that Chlorella went more “readily” from a unicellular to a viable multicellular form than vice versa. Which is interesting, certainly. But does it conflict with a mutation & selection scenario? Not at all. There’s absolutely no reason why the two transitions should average the same amount of time to occur.

[[[[[There’s a concept used by molecular and evolutionary biologists called the ‘molecular clock’. This ‘clock’ is predicated on a UNIFORM rate of mutation in all organisms. You can fight it out with them. This is just current evolutionary theory.]]]]]]]

Think about it. What factors affect the likelihood of a given phenotypic change due to mutation? Well, among other things:
1) the size of the population (bigger population = larger mutation rate),
2) the number of possible mutations that could produce said phenotypic change, and
3) the location of those mutations in more or less easily damaged parts of the genome.
Now 3) we can probably rule out here, since wherever a mutation could occur to induce multicellularity, presumably a second mutation at the same location could reverse it. But 1) is definitely a factor: we know that the colonial morph is outcompeted by the unicellular morph in the absence of predation, so it must have a lower reproductive rate—therefore its steady-state population in a given chemostat will be smaller. Moreover the colonial monocultures were recently grown, from a few Chlorella that must have been hand-selected to make sure they were colonial.

[[[[[[[[Sorry. From the paper: Initially, the culture tube was filled with medium and inoculated with Chlorella vulgaris Beij obtained from the University of Texas Culture Collection (UTEX #26). A steady state was established for the alga, which was then available as food to the flagellate predator. In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continuous cultures.”]]]]]]

So the present and past colonial population sizes were necessarily smaller than the same for the unicellular morph, therefore by 1) mutations should be less common.
As for 2), well, we don’t know much of anything about the exact mutations involved here. But there are many scenarios that would make unicellular-to-multicellular mutations more numerous than the reverse. For instance, we know that one of the mechanisms inducing colonialism here is incomplete breakdown of the mother cell wall after division. Suppose Chlorella’s got a gene which codes for an enzyme which breaks down that wall? Many mutations could inactivate that gene or severely disrupt enzyme function, say by frameshift; a much smaller number could reverse that effect. (IDers should be plenty familiar with that argument! “Mutations are always harmful,” right?)
Of course I just made that possibility up. But that’s the point—many possibilities exist for the precise mechanism producing the mutant colonial phenotype, and unless you can somehow rule most of them out, you can’t make any claims for how fast the colonial morph “should” be able to produce a viable unicellular mutant.
So…while it’s certainly worth looking into as to why the colonies didn’t mutate to unicellular morphs as rapidly as vice versa, it has no bearing on whether a mutation/selection model actually works here.

[[[[[[I disagree. The fact that ‘mutation’ is unidirectional has a tremendous bearing on how to interpret these results. As I said before: “what’s good for the goose, is good for the gander.” It’s more than just a little convenient to invoke a mechanism that relies on ‘mutations’ when they’re needed and “wanted”, and then disregard this same mechanism when it becomes problematic. Or is this just a case of looking the other way, “ because—well, otherwise you’d have to admit error, I suppose.”]]]]]]]]]]

Finally, Anton, these posts are getting exceedingly long. In your response, just pick out the major points you want to question or dispute. Pace.

Comment #82810

Posted by Anton Mates on February 28, 2006 10:17 PM (e)

BlastfromthePast wrote:

Finally, Anton, these posts are getting exceedingly long. In your response, just pick out the major points you want to question or dispute. Pace.

Sorry, I’m not trying to drive you to exhaustion! I’ll try to avoid redundancy, but I think it’s necessary to examine the details. Major points are generally made in science by assembling a wealth of supporting evidence–to critically analyze them, you’ve got to look at each piece one by one. Short & sweet knock-down arguments are more a feature of mathematics.

I’ll break up my response into two posts for better legibility, though. First, concerning your induction theory:

OK, but these experiments took place in chemostats, so how the mechanism works in the “real world” isn’t very relevant.

You mean we should just block out what nature might be telling us about the feasibility of this proposed scenario?

But nature isn’t telling us anything at this point. This entire business about chemical inducers and regions of high concentration is you idly speculating about nature without observational data. Different thing.

If you want to set up a study where you try to observe a similar effect in nature, more power to you–but the data here is from an experimental environment, and must be explained through mechanisms applicable within that environment.

You still need to explain why, with even low densities of predators (therefore low B, right?) and large numbers of the unicellular morph (therefore high A), the colonies still arise and persist. Remember, in the two-stage chemostat there’s a ton of unicellular Chlorella in the first stage, and any substances they’re pumping out will get carried along with them into the second stage.

Here’s a quote from the paper: ”Flagellates and Chlorella unicells in this steady state had population densities reduced to about 0.1% of their maximum numbers during the transient phases.” So “A” did not outnumber “B”.

That quote only refers to the chemostats which have flagellates in them, such as the second stage of the two-stager. In the first stage, there are no flagellates and the Chlorella’s all unicellular. The introduction of flagellates and development of colonies in the second stage does not affect the first stage, where the unicells are still happily thriving and pumping out your substance “A.” And, I might add, they vastly outnumber any organism in the second stage when colonies first appear, since that’s just after a population crash in the latter.

It would be quite reasonable—certainly plausible—that the ‘mother cell wall’ would reduce the amount of light that the ‘unicell’ (more or less) Chlorella would receive. So, in a low light situation, the ‘colonial’ form, lacking the ‘energy’ needed for cell division, just couldn’t keep up with the true unicell Chlorella (thus leading to ‘washout’), irrespective of whatever signaling was taking place.

Actually, washout in low light suggests to me that the colonies’ disadvantage is in nutrient uptake rather than photosynthesis–low light forces them to fall back on the medium for their energy needs, and then they get outcompeted fast, whereas when the light’s on they do almost as well as the unicells because both are relying on photosynthesis. But that’s just a minor point; I think we’re agreed that this at least was a selection effect.

From some other reading, it appears that a likely candidate for inducer “B” is simply something that spills out of the unicell form when it’s eaten by the flagellate. Thus, even “B” is not anything that has to be produced via an exceptional route. And as I stated above, the light-reducing effect of the mother cell wall is enough to explain the ‘washing out’ of the colonial form. So, we’re left with really one new chemical inducer, “C”, which likely affects the adhesive properties of daughter cells to the mother cell wall. Very simple, really.

That’s like saying “I believe an angel keeps the Earth in its orbit…and I’m not hypothesizing any new entities, because the angel is actually Michael Stipe.” Whether you’re claiming the existence of hitherto unknown inducers A and B, or identifying some known substances (byproducts of metabolism vs. death, or whatever) as A and B, you’re multiplying hypotheses either way.

Beyond that, you need many more hypotheses to explain what A, B and C actually do. For one thing, there are all these hysteresis effects you require–one substance will “flip a switch” making the organism either ignore or pay attention to another. And then there’s whatever network you think accounts for the change in distribution of colony sizes over time. And even if you accept that the colonies’ disappearance when the lights go out is due to a selection effect (as Boraas does), induction isn’t off the hook; you have to explain why the unicells entering the darkened, predator-filled second stage aren’t induced to become colonial anyway. After the original colonies washed out, the later unicells didn’t become colonial and then wash out in turn; they simply didn’t become colonial in the first place. So you still need your induction system to be photosensitive. Anything but “simple…”

Oh, and the system also has to account for the small but persistent population of unicells even in the flagellate-filled cultures.

But ID certainly doesn’t put limits on the information-processing capacity of genetic life.

No, it certainly does not….

Did I say the ‘rules of physics’, or simply ‘physics’. No, the ‘rules’ didn’t change; but the volume/surface area sure changed as the Chlorella went from unicell to 8-cell, to….100-cell forms. Are you making a concerted effort to misunderstand what I’m saying?

No…but I’m having trouble figuring out what you’re saying that Boraas didn’t say already (and I said several times). Yes, different-sized colonies have different nutrient-absorption efficiencies due to the volume/surface area relationship. Yes, the 8-celled morph is the most efficient of the colonies which are still large enough to avoid predation (and apparently 4 cells is large enough to avoid some predation, and even more efficient, so a few 4-celled forms stick around). So…how and why does the population first produce colonies of many different sizes and then converge on 8 cells?

The evolutionary explanation is: random mutations produce different-sized colonies and reproductive competition pares the colony size range down to the optimum (or close to it). Your explanation seems to be: the induction system uses some pseudorandom algorithm to try out various colony sizes, then the colonies all communicate with each other about how well they’re doing and switch over to the optimum size.

As to “mutation followed by selection…”; well, if it’s ‘induction’, then it’s not ‘mutation’.

Sure, but if it looks like mutation followed by selection, that’s a far more parsimonious hypothesis than “a complicated system of inducers and signals that happens to look exactly like mutation followed by selection.”

Comment #82815

Posted by Anton Mates on February 28, 2006 10:38 PM (e)

Now, on to general biological errors & whatnot.

We’re getting a little nasty here, aren’t we?

Must you always attack?

Your complaints of ad hominem arguments are rather amusing, given that you previously accused the paper’s primary author of having no motivation to really understand this phenomenon, because he only cares about upholding his Darwinian ‘faith’ and “winning plaudits.”

Nonetheless, I’m honestly not trying to insult you. It’s simply important for casual readers of this thread (assuming there are any, poor bastards) to understand that you’re not a very reliable source of information on biology. I point out your lack of expertise and failure to accurately read & report on papers so that no one else can be misled, not to offend you. It could be worse; I could be Lenny.

But I would quibble with you quite heartily over the term ‘evolution’—again, what ‘new’ form has been brought about; it would seem we just have ‘unicell’ Chlorella (same as before) that are kept inside the mother cell wall.

Quibble of my own: cell-wall containment was suggested as an initial mechanism for holding them together, but almost certainly isn’t the only one involved. In mature colonies the wall’s largely disintegrated and couldn’t bind the cells as tightly as one could see in the slides. Presumably, as Boraas mentions, there’s also adhesion of the daughter cell walls to one another.

And yes, these colonies are just a bunch of single cells bound together; but then so are we! True, multicelllular organisms usually have some cellular differentiation–even slime molds do–but even I’d be amazed if we saw that much evolve in a matter of weeks.

Here’s a quote from Pim’s post #80680: “You may misunderstand evolutionary theory here. Mutations do not happen because they are needed but rather mutations are present in the original stock and are selected for.” Does this sound like Pim was saying it “could have been there prior to the flagellate introduction”?

Yes. Pim says “original stock,” not “stock before the flagellate introduction or “stock at the time of culture creation” or “stock at some particular time T.” He was simply refuting your statement that “the right mutation has to occur at the right place, at the right time.” His point is that the mutation has to occur before selection can act on it, and is not caused by selection pressures.

I’m dead sure Pim would not claim that the mutations must have occurred either before or after the flagellate was introduced. Pim, care to chip in if you’re still watching? Regardless, I’m not claiming that.

Well, what was preventing the colonial form from multiplying into a larger percent of the total population before the predator appeared? Well, you’ll say, the unicell form is more ‘fit’ than the colonial form. Okay, that’s reasonable. But why is the ratio a million to one in an ambient where nutrient and light were available (stage one chemostat)?

Huh? What ratio? Do you mean relative fitness? And where did you get “a million to one” from?

I’m afraid I got it from you. You threw out the number upthread somewhere.

I’m not seeing it. I mentioned something about “millions of mutations,” but I have no idea how that equates to a “ratio of a million to one,” and I still don’t even know what ratio you’re talking about.

Neither morph has to be a million times fitter than the other in the current environment to displace it…it only has to be 1.000000001 times fitter!”

I’ll assume that the two ‘morphs’ of Chlorella, in stage one, compete for the Nitrogen. Otherwise, this wouldn’t be true.

They compete for everything. Nutrients, oxygen, light, space. Even if they had completely different nutritional requirements they’d trivially come into competition once they filled up the entire medium….

Blast-Past wrote: “It would be nice to have the data concerning how, and under what conditions, and to what degree, the unicell was more ‘competitive’ than the colonial—but, the data was not published. How interesting.”

That’s more than enough data to publish on.

Yes, but they wrote: “In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the light, the multicellular from was slowly displaced by unicells (data not shown).” p.160 Do you see my point now?

I guess; I just don’t think it’s a very strong one. Yes, there’s additional quantitative data it would be nice to have. There always is when a paper’s published. But they had a truckload of other stuff to write about, so I’m content with “slowly.”

Therefore, it can be predicted that even under high predation pressures, the unicellular morph population will stabilize short of total extinction, whereas if predation pressure’s absent, nothing stops the colonial morph from washing out completely.
Which is, you’ll note, precisely what happens.

So that proves that the normal form of Chlorella outside of predation is the unicell. But, of course, we already knew that.

That’s only the second half of my sentence above. What we didn’t know–but what evolutionary theory also predicts–is the first half.

So, big picture, according to your view, the so-called ‘mutation’ is already there, but not multiplying. Then the predator comes along, and it multiplies exponentially. Sounds like a triggering mechanism is in place.”

When you say things like that, it makes it very hard to believe you took several biology courses. Any organism multiplies exponentially if there’s room for it to do so—did you really not know that? And of course there is room in this case—the colonial morph becomes dominant immediately after a population crash due to predation, which leaves the culture wide open to repopulation.

Why do you focus in on the “exponential” part? And why do you even begin to suspect that I don’t know something as elementary as that?

Because you mentioned it as if it was somehow significant or unusual and implied a need for a triggering mechanism. Since you apparently know that it’s not and it doesn’t, why mention it?

Ok, the next part will take some time to correct, so let me put this up now.

Comment #82824

Posted by Anton Mates on March 1, 2006 1:28 AM (e)

Biological Errors part II: The Revenge!

BlastfromthePast wrote:

The point is that ‘according to your view’, what wouldn’t ‘grow’ before is now ‘growing’. So WHAT caused it to start ‘growing’? IOW, what ‘triggered’ the growth response? If the ‘unicell’ form has to only be 1.000000001 fitter than the ‘colonial’ form to outcompete it (your numbers), then why all of a sudden does it start to ‘outcompete’ the unicell form? Please explain. Remember that (1) ‘low’ unicell also results in ‘low’ predator, and (2) ‘low’ unicell means 0.1 % of its maximum density. Therefore, if the ‘mutant’ form exists, the ‘unicell’ has only declined in numbers by 10^3, whereas its fitness factor , relative to the colonial form (using your numbers) is 10^8. So the ‘colonial’ form should still be ‘outcompeted’—according to your logic.

Oh dear. The above really makes no sense at all. OK, Population Genetics 101:

The “fitness” of an organism is a measure of how successful it will be in producing offspring. If organism X is fitter than organism Y, it’s expected to leave behind more kids (or kids that are themselves more fecund or so forth). The greater the fitness difference, the more rapidly the population of X grows relative to that of Y. This can be expressed through “relative fitness,” which is–I’ll say for the sake of this discussion–the ratio of the two fitnesses (although there are lots of formulations, most of which I know nothing about). A fitness difference of zero (or relative fitness of 1 by my definition) means the populations grow at an equal rate.

Note that this has nothing to do with the actual proportions of X and Y at any given time in the population. Nothing. It just tells you how they’re changing, and how fast. X may start out as .0001% of the population, and if it is consistently fitter than Y–even if it’s only 1.0000000001 times fitter–it will eventually take up 100% of the population and (since population size is finite) Y will go extinct. The smaller the fitness difference, the longer it takes for this to happen, but it’ll still happen. The only way X and Y can stably coexist in the population is if their fitness difference is zero at the steady-state proportions. Of course, if the populations of X and Y change and then stabilize, that means their relative fitness is changing over time.

So trying to compute a “fitness factor” from steady-state population counts, or from the difference between them and the initial counts, or whatever it is you were doing above, is…well, it sure ain’t population genetics. By its very existence a steady state (even with mild fluctuations) implies an average fitness difference of zero (relative fitness of 1).

Now, let me explain how we’d view this system in terms of fitness. In the absence of the predator, but in strong light, the unicell is slightly fitter than the colony, and this fitness difference is more or less constant w. respect to the populations of the two morphs, because it’s due to things like their respective nutrient absorption efficiency, and that’s not population-size-dependent. Therefore, if you have a culture of the two morphs, the colonies go extinct–“slowly,” because the fitness difference isn’t that big, but inexorably.

In the presence of the predator, and at most population densities, the colony is fitter than the unicell–but its relative fitness decreases as its proportion in the population increases. Again, this is predictable, since a high colony density means a low predator density means unicells do better. When unicells are really rare, their now-fairly-minor-predation weakness balances with out their Mad Nutrient Absorption Skillz™, and their fitness breaks even with that of the colonies. With no fitness difference, the relative population sizes balance out and you have the observed steady state with lots of colonies and a small but permanent population of unicells and predators.

Chlorella isn’t zooplankton.

But it’s closely related.

a) zooplankton is an ecological category, not a phylogenetic taxon, so it’s fairly meaningless to say it’s “related” to anything, and
b) most zooplankton species are way more closely related to us than to Chlorella, being actual metazoan animals.

Again, if you want us to believe you took bio courses…

Why this tendency to prejudge? If you’ll look at an earlier post, you’ll see that I called Chlorella an algae.

Which means it really isn’t zooplankton.

And yeah, the conservative a priori guess would be that this was induction. That’s why Boraas took the time to rule that out.

Has he, in fact, ruled it out? Here’s a quote: “Our results could be interpreted as evidence that the flagellates released a substance inducing colony formation in Chlorella, ……..We discount this alternative hypothesis, based on four observations……”p.159 He ‘discounted’ it; he didn’t ‘rule it out.’ This isn’t just semantics here.

You’re right, actually–I take that back. The induction hypothesis is unfalsifiable at least until we have a near-total understanding of the Chlorella genome, so it can’t actually be ruled out. However, it can be shown to be unnecessary and therefore discounted for reasons of parsimony, and Boraas did that.

It’s not ‘evolution’, since what was there at the end, was there at the beginning

1) There’s no reason to think the colonial mutants that became successful were present from the beginning.
2) Even if they were, change in the frequencies of pre-existing alleles is still evolution. You know this. You’d call it “micro-evolution,” and it certainly wouldn’t be as interesting a case as what did happen here, but it would be evolution.

Yes. It would be an ‘interesting case’, IF that’s what happens. But aren’t we arguing over exactly what did happen? Why jump the gun?

Because, for Cthulhu’s sake, you just said “it’s not ‘evolution’, since what was there at the end, was there at the beginning,” and that characterization of evolution is simply wrong. Irrespective of what happened in this experiment, it’s wrong. IDers, YECers, and border collies all know that. So I corrected you.

3) “So-called mutations” did not hit on the same defense mechanism 70% of the time—no one’s suggesting they did except you. And you know this too, because you paraphrased me as saying “1 in a million” previously. You’re simply choosing to ignore that and return to your “70% of cultures featured 8-celled forms —> 70% of mutations produced 8-celled forms” claim because—well, otherwise you’d have to admit error, I suppose.

Please pay attention. Here’s a quote: ”After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

Here’s another quote: “We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.” Obviously Boraas is only referring to the replicates where colonies actually happened in the sentence you quote above. There’s a small amount of ambiguity in that particular sentence, but if you actually read the entire paper it’s very clear.

Of course you still haven’t explained why you continue to claim that “70% of cultures have 8-celled mutants” implies “70% of mutations produce 8-celled forms” when you know this is false.

(My emphasis) Please explain how the ‘solution’ to the ‘problem of a predator’ is solved in the same way each and every time the experiment is tried? This I’ve got to see.

It isn’t solved the same way, of course, as we see from the initial diversity in colony sizes. A truckload of possible solutions are presented by good ol’ random mutation. 30% of the time no mutation occurs which offers a viable colonial form–kind of what you’d expect since mutations are random–and the unicells win the day. The rest of the time colonies arise, further mutate and diversify, and natural selection, which is obviously non-random, picks the best–which are, predictably, going to be those with 8 or so cells.

Which isn’t really unexpected, given how you danced around the issue of the “kind” of Helacyton gartleri in an earlier thread, but is rather depressing.

We’re getting a little nasty here, aren’t we? Here’s an answer: a “kind” is a “paradigmatic form”. Okay? As if I really need to explain what it is. Shall I explain what a chair is also? I bet you know one when you see one.

And here we go again–assorted irrelevancies but no answer whatsoever to the question of what “kind” H. gartleri is, whether the “human kind” or some other. I’d ask again, but I lack Lenny’s stamina in asking questions that will never get answers.

Are you, by any chance, referring to this statement: p.159/160 “The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have been maintained for several months.” My reading of this is that the ‘several months’ refers only to the chemostats kept at steady states. You’re wrong here, and that affects the argument you construct below.

You mean you think the agar and whatever non-cycled liquid cultures lasted longer than that? When there’s no evidence for that, and chemostats are designed for long-term rapid reproduction while agar is not, and Boraas is trying to make a point about how long the colonies bred true for? He actually happened to have some really active colonies on agar for years or something and just forgot to mention it? That makes no sense.

On top of that, the average time-to-appearance of the colonial morphs was not 10-20 generations—that was the time it took for the eight-celled morph to dominate the culture after the appearance of colonies.

Rather, “colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates,”

I don’t see the difference between what you’re saying and the quote above that is taken from the paper: “After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph….p. 160 The ‘inoculation’ introduced the ‘presence’ of the phagotroph.

Yes. But the above sentence is saying that the eight-celled colony had to spend 10-20 generations in its presence before selection drove it to dominance. (Which should be obvious from the fact that the previous sentence is about how this experiment demonstrates the selection). It’s not saying anything about how long it took for there to be eight-celled colonies in the first place. Like Pim was saying, first you need the mutation, then selection can act on it.

Now it’s definitely the case that Chlorella went more “readily” from a unicellular to a viable multicellular form than vice versa. Which is interesting, certainly. But does it conflict with a mutation & selection scenario? Not at all. There’s absolutely no reason why the two transitions should average the same amount of time to occur.

There’s a concept used by molecular and evolutionary biologists called the ‘molecular clock’. This ‘clock’ is predicated on a UNIFORM rate of mutation in all organisms. You can fight it out with them. This is just current evolutionary theory.

…and now we know you were lying when you said you took genetics, unless you took it in the ’50s. Every intro genetics student learns about non-uniformity in mutations. Transitions are more common than inversions. Deletions are more common than insertions. Different parts of a chromosome will be more or less vulnerable. Different organisms have vastly different average mutation rates.

I mean, here. A Google Scholar search for “mutation rates.”. Same search in Nature. No one thinks there’s a universal, uniform mutation rate.

All “molecular clock” models require is the much weaker assumption that the average mutation rate, in certain areas of the genome (usually ones believed not to be under strong selection), in a particular lineage, during a particular timespan, was roughly constant. Sometimes that assumption pans out. Sometimes it doesn’t. But no biologist not currently in a straitjacket believes that every single possible mutation is as likely to occur as any other mutation.

(And of course even if that was the case, as I said before, we have no idea how many mutations correspond to a particular phenotypic change, so some sort of “equal probability of a phenotypic change and its inverse” principle would still be completely unsupportable.)

Moreover the colonial monocultures were recently grown, from a few Chlorella that must have been hand-selected to make sure they were colonial.

Sorry. From the paper: ” Initially, the culture tube was filled with medium and inoculated with Chlorella vulgaris Beij obtained from the University of Texas Culture Collection (UTEX #26). A steady state was established for the alga, which was then available as food to the flagellate predator. In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continuous cultures.”

Thanks for proving my point. The original culture has been at steady-state for twenty years. The colonial cultures, not. Which has had more chance to accumulate mutations, do you think?

I disagree. The fact that ‘mutation’ is unidirectional has a tremendous bearing on how to interpret these results. As I said before: “what’s good for the goose, is good for the gander.”

Folk proverbs do not substitute for actual well-supported principles of biology. If you have a personal “for any two populations, the probability of a mutation-induced phenotypic change in one is equal to the probability of the reverse change in the other” principle, wonderful. Paint it on a placard and parade it downtown. But you didn’t get that from evolutionary theory.

Comment #83431

Posted by BlastfromthePast on March 2, 2006 10:54 PM (e)

Anton says:

Blast wrote:

Anton Mates wrote:
OK, but these experiments took place in chemostats, so how the mechanism works in the “real world” isn’t very relevant.

You mean we should just block out what nature might be telling us about the feasibility of this proposed scenario?

But nature isn’t telling us anything at this point. This entire business about chemical inducers and regions of high concentration is you idly speculating about nature without observational data. Different thing.

This is tedious nit-picking on your part, Anton. To pursue a thought experiment to see if chemical induction could take place in “nature” is not a worthless pursuit. Why the bitching and moaning?

Anton then responds:

Blast responds:

Anton writes:
You still need to explain why, with even low densities of predators (therefore low B, right?) and large numbers of the unicellular morph (therefore high A), the colonies still arise and persist. Remember, in the two-stage chemostat there’s a ton of unicellular Chlorella in the first stage, and any substances they’re pumping out will get carried along with them into the second stage.

Here’s a quote from the paper: ”Flagellates and Chlorella unicells in this steady state had population densities reduced to about 0.1% of their maximum numbers during the transient phases.” So “A” did not outnumber “B”.

That quote only refers to the chemostats which have flagellates in them, such as the second stage of the two-stager. In the first stage, there are no flagellates and the Chlorella’s all unicellular. The introduction of flagellates and development of colonies in the second stage does not affect the first stage, where the unicells are still happily thriving and pumping out your substance “A.” And, I might add, they vastly outnumber any organism in the second stage when colonies first appear, since that’s just after a population crash in the latter.

Have you thought through what it means that both ‘unicells’ and ‘predators’ were at 0.1% of their maximum? The only possible explanation is that the “flow rate” from the 1st Stage to the 2nd Stage is highly restricted. That’s the only way you can keep the populations down. Therefore, there’s NOT an ‘abundance’ of substance “A”; rather, they’re present in almost equal amounts.

Anton gets in the last word (or did he?):

Blast responds to Anton:

Anton responds:

Blast wrote:It would be quite reasonable—certainly plausible—that the ‘mother cell wall’ would reduce the amount of light that the ‘unicell’ (more or less) Chlorella would receive. So, in a low light situation, the ‘colonial’ form, lacking the ‘energy’ needed for cell division, just couldn’t keep up with the true unicell Chlorella (thus leading to ‘washout’), irrespective of whatever signaling was taking place.

Actually, washout in low light suggests to me that the colonies’ disadvantage is in nutrient uptake rather than photosynthesis—low light forces them to fall back on the medium for their energy needs, and then they get outcompeted fast, whereas when the light’s on they do almost as well as the unicells because both are relying on photosynthesis. But that’s just a minor point; I think we’re agreed that this at least was a selection effect.

From some other reading, it appears that a likely candidate for inducer “B” is simply something that spills out of the unicell form when it’s eaten by the flagellate. Thus, even “B” is not anything that has to be produced via an exceptional route. And as I stated above, the light-reducing effect of the mother cell wall is enough to explain the ‘washing out’ of the colonial form. So, we’re left with really one new chemical inducer, “C”, which likely affects the adhesive properties of daughter cells to the mother cell wall. Very simple, really.

That’s like saying “I believe an angel keeps the Earth in its orbit…and I’m not hypothesizing any new entities, because the angel is actually Michael Stipe.” Whether you’re claiming the existence of hitherto unknown inducers A and B, or identifying some known substances (byproducts of metabolism vs. death, or whatever) as A and B, you’re multiplying hypotheses either way.
Beyond that, you need many more hypotheses to explain what A, B and C actually do. For one thing, there are all these hysteresis effects you require—one substance will “flip a switch” making the organism either ignore or pay attention to another. And then there’s whatever network you think accounts for the change in distribution of colony sizes over time. And even if you accept that the colonies’ disappearance when the lights go out is due to a selection effect (as Boraas does), induction isn’t off the hook; you have to explain why the unicells entering the darkened, predator-filled second stage aren’t induced to become colonial anyway. After the original colonies washed out, the later unicells didn’t become colonial and then wash out in turn; they simply didn’t become colonial in the first place. So you still need your induction system to be photosensitive. Anything but “simple…”
Oh, and the system also has to account for the small but persistent population of unicells even in the flagellate-filled cultures.

You appear completely unable to understand a very simple statement. The response I made concerning substance “C” indicates that the only ‘substance’ different than those normally present is “C” alone. That simplifies things, no matter how much you mutter on.

You keep talking about ‘hysteresis’, which is normally used to describe a system that is out of equilibrium. So, frankly, I don’t know why you don’t prefer a straightforward chemistry term such as ‘activation energy.’ Added to this is the fact that we KNOW that chemical induction takes place between zoo-plankton and phyto-plankton. So, somehow, this ‘hysteresis’ that you’re so hysterical about does, indeed, take place. Search the literature: it uses the term “trigger.”

As to the last part regarding the ‘darkened second stage’, it’s really hard to figure out what you’re talking about. The light is reduced, the colonies are deprived of energy, they can’t keep up their reproduction and motility, so they are ‘washed out’. That leaves ‘unicell’ and predator (probably at low levels). Based on what’s already been seen, the unicells would have to first increase their density dramatically, then the predator would have to ‘graze’ them down, and then the ‘colonial’ form would show up again. Is that about 20 days? Well, maybe the best explanation is that they decided to stop the experiment before all of that happened. That leaves…..let me see…..nothing to explain.

Anton:

Blast wrote:
But ID certainly doesn’t put limits on the information-processing capacity of genetic life.

No, it certainly does not….

So, you agree. Maybe there’s hope for you.

Anton responds:

Blast wrote:
Did I say the ‘rules of physics’, or simply ‘physics’. No, the ‘rules’ didn’t change; but the volume/surface area sure changed as the Chlorella went from unicell to 8-cell, to….100-cell forms. Are you making a concerted effort to misunderstand what I’m saying?

No…but I’m having trouble figuring out what you’re saying that Boraas didn’t say already (and I said several times). Yes, different-sized colonies have different nutrient-absorption efficiencies due to the volume/surface area relationship. Yes, the 8-celled morph is the most efficient of the colonies which are still large enough to avoid predation (and apparently 4 cells is large enough to avoid some predation, and even more efficient, so a few 4-celled forms stick around). So…how and why does the population first produce colonies of many different sizes and then converge on 8 cells?
The evolutionary explanation is: random mutations produce different-sized colonies and reproductive competition pares the colony size range down to the optimum (or close to it). Your explanation seems to be: the induction system uses some pseudorandom algorithm to try out various colony sizes, then the colonies all communicate with each other about how well they’re doing and switch over to the optimum size.

Well, first of all, I was responding to your misunderstanding of what I was referring to as ‘physics’. Why make it sound like more than that? I don’t understand.

Now, as to the explanation of differing ‘colony’ sizes, here goes: when the first signal for colony formation comes, the Chlorella ‘mother cells’ continue to produce more and more ‘daughter cells’ before they, basically, ‘burst.’ When they do ‘burst’, the ‘daughter cells’, instead of going off ‘alone’, cling to the mother cell’s membrane (wall). This results in ‘colonies’ of various sizes, large and small. Then, after the Chlorella begin to respond to a steady signal, they exit this transitory system and begin to produce predominantly 8-cell colonies. Rather straightforward, don’t you think?

Now, you think your explanation is so simple. But according to RM+NS, you have to explain why there is a 100-cell colony, why an 8-cell, why a 4-cell. That’s THREE mutations—out of the clear-blue sky. Yet, colonial Chlorella breeds true for months. Interesting.

Anton responds:

Blast wrote:
As to “mutation followed by selection…”; well, if it’s ‘induction’, then it’s not ‘mutation’.

Sure, but if it looks like mutation followed by selection, that’s a far more parsimonious hypothesis than “a complicated system of inducers and signals that happens to look exactly like mutation followed by selection.”

Help me out here……..aren’t ecosystems complicated? Aren’t the interactions that take place there complicated? So is it really a surprise that a rather ‘simple’ system of communication takes place?

Comment #83447

Posted by Steviepinhead on March 3, 2006 12:17 AM (e)

Memo to Blast:

Hey, kid, Ghost of Paley–stooping to steal a page from the Book of Larry–is mimicking you. Ya better fill the internet lines with the fear and trembling of your retro presence until Ol’ Ghosty ceases and desistses.

Up with Psuedo-Blasts, we will not put! That would be like letting Lenny’s Pizza Guy get away with a slow pasta delivery to Lenny, based on the whine that Lenny loaned him a leaky kayak, resulting in sore shoulders and a general bad attitude on the part of Pizza Guy… We don’t let anyone get away with whining or deceiving, not the evo-devo good guys, and not even the regulars and, yes, the protection of our “anti-deception policy” most certainly likewise embraces our favorite trolls: youse wise guys better not crowd in here trying to poach on our trolls, no siree ma’am!!

Comment #83456

Posted by BlastfromthePast on March 3, 2006 1:11 AM (e)

Anton answers:

Blast responds:

Anton wrote:
Now, on to general biological errors & whatnot.

We’re getting a little nasty here, aren’t we?
Must you always attack?

Your complaints of ad hominem arguments are rather amusing, given that you previously accused the paper’s primary author of having no motivation to really understand this phenomenon, because he only cares about upholding his Darwinian ‘faith’ and “winning plaudits.”
Nonetheless, I’m honestly not trying to insult you. It’s simply important for casual readers of this thread (assuming there are any, poor bastards) to understand that you’re not a very reliable source of information on biology. I point out your lack of expertise and failure to accurately read & report on papers so that no one else can be misled, not to offend you. It could be worse; I could be Lenny.

You’ve mischaracterized what I said about the author. It was not an ad hominem.
It was merely pointing out that, from a RM+NS point of view, there was no motivation to ask further questions. I think that’s a fair enough observation. You, on the other hand, want to prove that I am “not a very reliable source of information on biology.” That’s an ad hominem. And it is the height of ironies that you want to point out my “failure to accurately read & report on papers” when I’ve pointed out to you—twice already—that you’ve misunderstood the causation behind the ‘washing out’ of the colonial form in the darkened 2nd Stage, among other errors.

Anton responds:

Blast wrote:But I would quibble with you quite heartily over the term ‘evolution’—again, what ‘new’ form has been brought about; it would seem we just have ‘unicell’ Chlorella (same as before) that are kept inside the mother cell wall.

Quibble of my own: cell-wall containment was suggested as an initial mechanism for holding them together, but almost certainly isn’t the only one involved. In mature colonies the wall’s largely disintegrated and couldn’t bind the cells as tightly as one could see in the slides. Presumably, as Boraas mentions, there’s also adhesion of the daughter cell walls to one another.
And yes, these colonies are just a bunch of single cells bound together; but then so are we! True, multicelllular organisms usually have some cellular differentiation—even slime molds do—but even I’d be amazed if we saw that much evolve in a matter of weeks.

Very simple explanation: Substance “C” causes the ‘unicells’ to adhere more strongly, membrane-to-membrane. This results in their ‘clinging’ to the mother’s ‘cell-wall’ and to one another.

Let’s look—once again—to the ‘big picture’: In the ‘beginning’, there are mother cells, daughter cells, and mother cell walls. In the ‘end’, there are mother cells, daughter cells, and mother cell walls. So, tell me, what has ‘evolved’? It appears that the cell membranes of the unicells have become more sticky. Is it a ‘chemical’ response? I think so. Something has ‘changed’; but nothing has ‘evolved’. (Please don’t bore me with an argument that wants to equate the two. Thank you.)

Anton responds:

Blast wrote:
Here’s a quote from Pim’s post #80680: “You may misunderstand evolutionary theory here. Mutations do not happen because they are needed but rather mutations are present in the original stock and are selected for.” Does this sound like Pim was saying it “could have been there prior to the flagellate introduction”?

Yes. Pim says “original stock,” not “stock before the flagellate introduction or “stock at the time of culture creation” or “stock at some particular time T.” He was simply refuting your statement that “the right mutation has to occur at the right place, at the right time.” His point is that the mutation has to occur before selection can act on it, and is not caused by selection pressures.
I’m dead sure Pim would not claim that the mutations must have occurred either before or after the flagellate was introduced. Pim, care to chip in if you’re still watching? Regardless, I’m not claiming that.

Pim hasn’t ‘chipped in’. Based on what I had written, the most reasonable interpretation of what Pim wrote is that which I ascribed to him. He didn’t have to use the term “original stock”; all he had to say was “the mutation arose before NS acted on it.”

Anton writes:

Blast returns the favor:

Anton responds:

Blast wrote:Well, what was preventing the colonial form from multiplying into a larger percent of the total population before the predator appeared? Well, you’ll say, the unicell form is more ‘fit’ than the colonial form. Okay, that’s reasonable. But why is the ratio a million to one in an ambient where nutrient and light were available (stage one chemostat)?

Huh? What ratio? Do you mean relative fitness? And where did you get “a million to one” from?

I’m afraid I got it from you. You threw out the number upthread somewhere.

I’m not seeing it. I mentioned something about “millions of mutations,” but I have no idea how that equates to a “ratio of a million to one,” and I still don’t even know what ratio you’re talking about.
Neither morph has to be a million times fitter than the other in the current environment to displace it…it only has to be 1.000000001 times fitter!”

Here’s what you wrote: “Nope, that’s neither what the data suggests nor what an evolutionary explanation requires. 70% of the cultures ended up mostly eight-celled—that simply means that one of the right mutations or combos of mutations has to occur in one of the millions of cells in 70% of your cultures.”

Is it now clear to you?

Anton says:

Blast wrote:
I’ll assume that the two ‘morphs’ of Chlorella, in stage one, compete for the Nitrogen. Otherwise, this wouldn’t be true.

They compete for everything. Nutrients, oxygen, light, space. Even if they had completely different nutritional requirements they’d trivially come into competition once they filled up the entire medium….

There’s plenty of nutrient—it’s being supplied. There’s plenty of light. There’s plenty of oxygen. Space may be limited. But the only mention of anything being ‘limited’ is in reference to nitrogen.

Anton orates:

Blast responds:

Anton writes:

Blast-Past wrote: It would be nice to have the data concerning how, and under what conditions, and to what degree, the unicell was more ‘competitive’ than the colonial—but, the data was not published. How interesting.

That’s more than enough data to publish on.

Yes, but they wrote: “In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the light, the multicellular from was slowly displaced by unicells (data not shown).” p.160 Do you see my point now?

I guess; I just don’t think it’s a very strong one. Yes, there’s additional quantitative data it would be nice to have. There always is when a paper’s published. But they had a truckload of other stuff to write about, so I’m content with “slowly.”

You’re content. Well, let’s think about this. In the presence of the predator (and unicell), the ‘colonial form’ persists. In a continuous culture, the ‘colonial form’ breeds true. (Where’s the mutations??) And then, lastly, you remove the predator (source of what ‘induces’ substance “C”) and the unicells ‘slowly’ displace the ‘multicellular’ forms.

So, when the source of “C” is removed, and the source of “A” is present, the colonials disappear.

When the colonial is all by itself, nothing happens. It continues undeterred.

All of this sounds like chemical induction.

If, indeed, this is induction, it is of more than passing interest to know the specifics as to how the “unicellular” form ‘displaced’ the “colonial form”.

Finally, tell me, Anton, did the ‘unicellular’ forms ‘induce’ a ‘mutation’ in the ‘colonial form’? Is that how the ‘colonial’ form was displaced?

Anton then writes:

Blast resonds:

Anton wrote:
Therefore, it can be predicted that even under high predation pressures, the unicellular morph population will stabilize short of total extinction, whereas if predation pressure’s absent, nothing stops the colonial morph from washing out completely.
Which is, you’ll note, precisely what happens.

So that proves that the normal form of Chlorella outside of predation is the unicell. But, of course, we already knew that.

That’s only the second half of my sentence above. What we didn’t know—but what evolutionary theory also predicts—is the first half.

I have no idea what the first part of your post means. How, and in what way, does what you state flow from what was carried out in this experiment? Why didn’t the authors come to this conclusion and present it as such? “Nothing stops the colonial morph from washing out completely”…….where is that stated? I only have a hint of what you might mean, and if you mean what I think you do, you’re simply ‘presuming’ this so as to salvage your argument.

Anton says:

Blast responds:

Anton writes:

Blast wrote:
So, big picture, according to your view, the so-called ‘mutation’ is already there, but not multiplying. Then the predator comes along, and it multiplies exponentially. Sounds like a triggering mechanism is in place.”

When you say things like that, it makes it very hard to believe you took several biology courses. Any organism multiplies exponentially if there’s room for it to do so—did you really not know that? And of course there is room in this case—the colonial morph becomes dominant immediately after a population crash due to predation, which leaves the culture wide open to repopulation.

Why do you focus in on the “exponential” part? And why do you even begin to suspect that I don’t know something as elementary as that?

Because you mentioned it as if it was somehow significant or unusual and implied a need for a triggering mechanism. Since you apparently know that it’s not and it doesn’t, why mention it?

Pay close attention: According to you, you have this ‘one (of the millions of) cell(s)’ that for some reason isn’t growing. Why not? Why isn’t it growing and multiplying? Because, you would answer, it is less fit than the ‘unicell’. Well, then, what happens to the cell? It dies. So there’s nothing to select. So, now where are we? You would respond that there are millions of cells. Surely one of those cells will ‘mutate’. OK. Millions of cells. What is an average mutation rate? Let’s assume it is one in 10^6/generation. So, at that rate, there’s always an array of mutations to choose from. [Should I now point out that EXPERIMENTALLY, over 99% of mutations are harmful. But we’ll neglect that since that seems to bother you.] But what kind of a mutation is it? Well, whether it is an ‘insertion’, or a ‘deletion’, or SNP, it happens at some position on the chromosome. How many positions are there in the chromosome? Probably upwards of 10^9. Therefore, what are the odds of the mutation taking place at just the ‘right spot’? 100x10^6 #of cells per generation/one in 10^6 mutations per division/10^9 locations for the mutation to occur. Drumroll please……The odds are 1 in 10^7; translated, one in 10 million. If the 100s of millions of cells per each generation is maintained, this will take 10 million generations to occur. How much time does that correspond to? 10 million days (more, or less). That is, approximately 30,000 years.

And yet we’re told that this occurs EVERY time they run the experiment. (Not just 70% of the time).

As to the ‘exponential growth’ that I referred to that seems like a ‘trigger’, well, let’s look at it this way. The predator is introduced, the unicell population drops precipitously. Then the predator population, in response to the unicell decline, declines itself to a very low level. Now, you say, there’s this ‘mutant’ (out of the 100’s of millions of cells). Now, all of a sudden, it decides to grow ‘exponentially’. Why? Why does it grow at all? You say that even if the unicell is only 1.000000001 as fit as the colonial, it will (from you latest post) “even if it’s only 1.0000000001 times fitter—it will eventually take up 100% of the population and (since the population size is finite) [the colonial form] will go extinct.” So, I repeat, I’m surprised that it ‘grows exponentially’. (Maybe something ‘triggered’ the response!)

Comment #83539

Posted by Anton Mates on March 3, 2006 1:30 PM (e)

BlastfromthePast wrote:

But nature isn’t telling us anything at this point. This entire business about chemical inducers and regions of high concentration is you idly speculating about nature without observational data. Different thing.

This is tedious nit-picking on your part, Anton. To pursue a thought experiment to see if chemical induction could take place in “nature” is not a worthless pursuit. Why the bitching and moaning?

Blast considers differentiating between “things we have seen in nature” and “things Blast thinks we might see in nature” to be “tedious nit-picking.” Noted.

And actually, thought experiments to see if Hypothetical Biological Phenomenon X could take place in nature are fairly useless. You’re almost always going to return the answer “Yeah, maybe.” Nothing wrong with thought experiments, of course, but you’ve got a real experiment with real data to start from….

Have you thought through what it means that both ‘unicells’ and ‘predators’ were at 0.1% of their maximum? The only possible explanation is that the “flow rate” from the 1st Stage to the 2nd Stage is highly restricted. That’s the only way you can keep the populations down. Therefore, there’s NOT an ‘abundance’ of substance “A”; rather, they’re present in almost equal amounts.

You raise a good point here, though not in the way you think. We don’t know that the unicells and predators in the 2nd stage were at .1% of their maximum. That quote comes before any mention of the two-stage chemostat, and all we’re told of the relative numbers in the latter is that “We see colonial Chlorella.” Moreover the nitrogen limitation means that the colonial population is directly dependent on the influx of new unicells to grow—the colonies require the nitrogen which is excreted by the predator after it eats the unicells, while nitrogen is constantly drained from the system by population loss through medium cycling. So the population of unicells can’t drop that far below the population of colonies, and your argument that there must not have been many unicells around to produce substance “A” collapses.

You appear completely unable to understand a very simple statement. The response I made concerning substance “C” indicates that the only ‘substance’ different than those normally present is “C” alone. That simplifies things, no matter how much you mutter on.

No, you claim that all your other hypothetical substances than “C” are ones which are normally present. That’s a big bundle of hypotheses. I know you equate your claims with empirical reality, but unfortunately it doesn’t work that way for the rest of us.

But I think we’ve established your concept of “simplicity” very well—it’s the Goddidit idea. “There’s a substance, and it accounts for everything we saw. Somehow.” Well, wonderful.

You keep talking about ‘hysteresis’, which is normally used to describe a system that is out of equilibrium. So, frankly, I don’t know why you don’t prefer a straightforward chemistry term such as ‘activation energy.’

Um, because ‘hysteresis’ is a more correct term? I’m not complaining about you using the term “activation energy” as a metaphor, but you do know it is metaphorical, right? Because Chlorella aren’t individual molecules?

Added to this is the fact that we KNOW that chemical induction takes place between zoo-plankton and phyto-plankton. So, somehow, this ‘hysteresis’ that you’re so hysterical about does, indeed, take place. Search the literature: it uses the term “trigger.”

Oh, I’m quite happy with hysteresis and chemical induction and the latter exhibiting the former. I just prefer people to actually provide evidence for it in each instance rather than daydreaming about how it would be really great if it happened.

There’s also the small fact that no observed example of hysteresis has ever been remotely this extreme. A unicell can be “induced” to go colonial, then removed from the inducer and left for months—hundreds of generations–in an environment identical to the original unicell’s without reverting? Nope.

Based on what’s already been seen, the unicells would have to first increase their density dramatically, then the predator would have to ‘graze’ them down, and then the ‘colonial’ form would show up again. Is that about 20 days? Well, maybe the best explanation is that they decided to stop the experiment before all of that happened. That leaves…..let me see…..nothing to explain.

Beautiful! But why don’t we simply argue that they never did the experiment at all, and simply bribed the journal to pretend that they did? That would leave nothing to explain even faster!

But ID certainly doesn’t put limits on the information-processing capacity of genetic life.

No, it certainly does not….

So, you agree. Maybe there’s hope for you.

Oh, I’m well aware that ID doesn’t put limits on anything except the explanatory power of naturalistic biology.

Now, as to the explanation of differing ‘colony’ sizes, here goes: when the first signal for colony formation comes, the Chlorella ‘mother cells’ continue to produce more and more ‘daughter cells’ before they, basically, ‘burst.’ When they do ‘burst’, the ‘daughter cells’, instead of going off ‘alone’, cling to the mother cell’s membrane (wall). This results in ‘colonies’ of various sizes, large and small. Then, after the Chlorella begin to respond to a steady signal, they exit this transitory system and begin to produce predominantly 8-cell colonies. Rather straightforward, don’t you think?

Good god, no. What distinguishes a transitory from a steady signal? Why does the transitory system involve these colonies of various sizes while the steady-state system does not? And why does the steady-state system seize on 8-cell colonies in particular? You haven’t explained any of this—you’ve just renamed the unknowns with labels like “steady signal” and “transitory system.”

Now, you think your explanation is so simple. But according to RM+NS, you have to explain why there is a 100-cell colony, why an 8-cell, why a 4-cell. That’s THREE mutations—-out of the clear-blue sky.

Three mutations! In a population that should really only have time for a paltry few million or so! Shocking.

Yet, colonial Chlorella breeds true for months. Interesting.

This is actually something I could legitimately see you getting confused about. The only things we know the colonies didn’t mutate back to in that timeframe are colonies of smaller size. It’s entirely possible, though, that they mutated to larger colonies and then washed out, just as all the colonies which appeared via mutation long before the predator’s introduction would have washed out.

And of course true breeding doesn’t mean absolutely no mutations of any sort. If it did, nothing on Earth could be described as breeding true.

Help me out here……..aren’t ecosystems complicated? Aren’t the interactions that take place there complicated? So is it really a surprise that a rather ‘simple’ system of communication takes place?

But you’re not attributing the complexity to the whole ecosystem, but rather to the chemical behavior of this one unicellular organism! Somehow it’s responsible for converting itself into a colonial form and trying out multiple sizes and then hitting on just the right one to avoid predation while absorbing nutrients and then holding itself at that size even after the predator’s gone until a bunch of its solitary brethren come by to convince it otherwise.

Sure, ecosystems are complicated, due to all the interactions. The world is complicated. But the problem with ID is that it doesn’t try to account for all that complexity by breaking it down into simpler interactions that can be examined and tested—it simply bundles it all into specific spots in the genome and from there into the Great Designer who can never be examined and tested.

Comment #83553

Posted by Anton Mates on March 3, 2006 2:28 PM (e)

BlastfromthePast wrote:

You’ve mischaracterized what I said about the author. It was not an ad hominem.
It was merely pointing out that, from a RM+NS point of view, there was no motivation to ask further questions. I think that’s a fair enough observation.

Um, maybe if you assume that any holder of “a RM+NS point of view” only cares about what “affirms his ‘faith’ in the theory and wins him plaudits.” As you said.

I mean, I don’t mind, I and others have said the same thing about plenty of creationists. It’s just silly of you to pretend that you’re not doing that sort of thing.

You, on the other hand, want to prove that I am “not a very reliable source of information on biology.” That’s an ad hominem.

Yep. And it’s a valid use of it because your arguments involve scientific and mathematical claims which, as I’ve shown, are generally incorrect or misunderstood. I take the trouble to demonstrate this because I don’t want everyone else to have to do the same.

And it is the height of ironies that you want to point out my “failure to accurately read & report on papers” when I’ve pointed out to you—twice already—that you’ve misunderstood the causation behind the ‘washing out’ of the colonial form in the darkened 2nd Stage, among other errors.

Lord help me, I’ve done everything in my power to explain to you how chemostats work and what “washing out” actually means. If it hasn’t worked, I hereby surrender.

I think so. Something has ‘changed’; but nothing has ‘evolved’. (Please don’t bore me with an argument that wants to equate the two. Thank you.)

Heh, argumentum ad tedium? I can understand how you’d find biological facts boring—they’ve been repeated to you in these arguments so many times!

I’m dead sure Pim would not claim that the mutations must have occurred either before or after the flagellate was introduced. Pim, care to chip in if you’re still watching? Regardless, I’m not claiming that.

Pim hasn’t ‘chipped in’. Based on what I had written, the most reasonable interpretation of what Pim wrote is that which I ascribed to him. He didn’t have to use the term “original stock”; all he had to say was “the mutation arose before NS acted on it.”

Well, you’re welcome to interpret Pim as you like—he can defend himself, I’m sure.

I’m not seeing it. I mentioned something about “millions of mutations,” but I have no idea how that equates to a “ratio of a million to one,” and I still don’t even know what ratio you’re talking about.

Here’s what you wrote: “Nope, that’s neither what the data suggests nor what an evolutionary explanation requires. 70% of the cultures ended up mostly eight-celled—that simply means that one of the right mutations or combos of mutations has to occur in one of the millions of cells in 70% of your cultures.”

Is it now clear to you?

It’s clear what I said, but why you responded with “But why is the ratio a million to one in an ambient where nutrient and light were available (stage one chemostat)?” I fear I shall never know. I mean, I assume you’re not saying that nutrients and light should somehow alter the probability of desirable mutations, but I don’t know what else you could mean.

They compete for everything. Nutrients, oxygen, light, space. Even if they had completely different nutritional requirements they’d trivially come into competition once they filled up the entire medium….

There’s plenty of nutrient—it’s being supplied. There’s plenty of light. There’s plenty of oxygen. Space may be limited. But the only mention of anything being ‘limited’ is in reference to nitrogen.

Space may be limited? The culture’s inside a 500 ml tube, not a pocket universe!
There are finite rates of input of nutrients and light, and a finite amount of space. Each organism makes use of a certain amount of each. Obviously once there are enough organisms, they run out of something; that’s why there’s a steady-state population! (Dumb of me to include “oxygen,” though, since the Chlorella can probably switch between mixotrophy and phototrophy as necessary depending on whether oxygen or CO2 gets low.)

You’re content. Well, let’s think about this. In the presence of the predator (and unicell), the ‘colonial form’ persists. In a continuous culture, the ‘colonial form’ breeds true. (Where’s the mutations??)

When the predator’s still around or when it’s not? Either way the answer’s the same—they’re busy appearing, then washing out, because they have lower fitness in the current environment.

And then, lastly, you remove the predator (source of what ‘induces’ substance “C”) and the unicells ‘slowly’ displace the ‘multicellular’ forms.

So, when the source of “C” is removed, and the source of “A” is present, the colonials disappear.

When the colonial is all by itself, nothing happens. It continues undeterred.

All of this sounds like chemical induction.

Except that that last bit about “when the colonial is all by itself, nothing happens” is completely unlike known cases of chemical induction. (Though you might be able to dredge up an analogous case of extragenetic inheritance.)

Finally, tell me, Anton, did the ‘unicellular’ forms ‘induce’ a ‘mutation’ in the ‘colonial form’? Is that how the ‘colonial’ form was displaced?

I can’t tell…are you being sarcastic? The obvious answer is “No, it was displaced by competition since the unicell population increased faster than the colonial population in the absence of the predator;” but I can’t believe you didn’t have something more profound in mind than that.

I have no idea what the first part of your post means.

Is “Therefore, it can be predicted that even under high predation pressures, the unicellular morph population will stabilize short of total extinction” really that hard to understand? Even with lots of predators, the unicells won’t disappear completely. Because selection pressure due to predation varies inversely with the unicell/colony ratio.

How, and in what way, does what you state flow from what was carried out in this experiment? Why didn’t the authors come to this conclusion and present it as such?

What, that predation pressure is usually density-dependent and this tends to stabilize prey species short of extinction? Why would they bother to say that? That’s Ecology 101. Heck, I tell my Diff Eq students about density-dependent population pressures, just as a real-world example, and they’re sophomore engineers!

Comment #83570

Posted by Anton Mates on March 3, 2006 5:46 PM (e)

I put the following in its own post, since it’s more strong evidence that Blast cannot possibly have taken the biology classes he claims to have taken. Unless he was taking heavy hallucinogens at the same time.

Pay close attention:

Oboy.

According to you, you have this ‘one (of the millions of) cell(s)’ that for some reason isn’t growing. Why not? Why isn’t it growing and multiplying? Because, you would answer, it is less fit than the ‘unicell’. Well, then, what happens to the cell? It dies. So there’s nothing to select.

No, no. It is growing, it is multiplying, just not quickly enough to compensate for the steady population loss as organisms get flushed out of the chemostat with the old medium. And the reason it’s not multiplying quickly enough is that is that the medium is already full to capacity with unicells, which are better at sucking up the available resources than the colonial mutant is.

So, now where are we? You would respond that there are millions of cells. Surely one of those cells will ‘mutate’. OK. Millions of cells. What is an average mutation rate? Let’s assume it is one in 10^6/generation.

Off by at least a factor of a thousand. I can’t find anything specific for Chlorella, but Drake et al. (1998, Genetics) finds a mutation rate of about 1 in 300/generation for various DNA-based unicellular organisms both prokaryotic and eukaryotic. (Higher eukaryotes have higher mutation rates, up to more than 1 per generation.)

So, at that rate, there’s always an array of mutations to choose from. [Should I now point out that EXPERIMENTALLY, over 99% of mutations are harmful. But we’ll neglect that since that seems to bother you.]

It certainly would bother me—and it’d bother all those silly geneticists who found that more than 90% of mutations are neutral. But maybe you can correct them.

Of course, it’s ironic that you bring up this old creationist chestnut, since the mutations we’re talking about were harmful—before the predator’s introduction changed the environment! Harmful is relative.

But what kind of a mutation is it? Well, whether it is an ‘insertion’, or a ‘deletion’, or SNP, it happens at some position on the chromosome. How many positions are there in the chromosome? Probably upwards of 10^9.

You mean “genome,” I think, not “chromosome”—eukaryotes have several chromosomes. And apparently the Chlorella genome’s a bit less than 10^8 bases long. (Not that the average bio major should know that! I had to look around some.)

Therefore, what are the odds of the mutation taking place at just the ‘right spot’?

And there’s the other real problem in your analysis. Who says there’s just one right spot? Why would there be? We’ve got at least two probable mechanisms here, if we want (let’s say) to get precisely 8-celled colonies—stickiness of the daughter cell walls and incomplete destruction of the mother cell walls. There are almost certainly hundreds or thousands of slight protein adjustments that would accomplish one or both of these to the right degree. Not even necessarily in the cell wall proteins themselves—maybe an enzyme that destroys the mother cell wall just has to work a little less effectively. Claiming only one mutation can possibly do the job isn’t even plausible.

100x10^6 #of cells per generation/one in 10^6 mutations per division/10^9 locations for the mutation to occur. Drumroll please……The odds are 1 in 10^7; translated, one in 10 million. If the 100s of millions of cells per each generation is maintained, this will take 10 million generations to occur. How much time does that correspond to? 10 million days (more, or less). That is, approximately 30,000 years.

Scary! Good thing that number’s at least a million or so times too large.

And yet we’re told that this occurs EVERY time they run the experiment. (Not just 70% of the time).

You keep saying this, and I keep looking at the paper and seeing

“We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.“

and…well, I can’t really complain, since admittedly I wanted to demonstrate that you misread papers, but…wow.

You say that even if the unicell is only 1.000000001 as fit as the colonial, it will (from you latest post) “even if it’s only 1.0000000001 times fitter—it will eventually take up 100% of the population and (since the population size is finite) [the colonial form] will go extinct.” So, I repeat, I’m surprised that it ‘grows exponentially’.

Um…you’re surprised that when the unicell stops being fitter than the colony—maybe goes from 1.000000001 to .99999999 times the colony fitness—the colony outcompetes it? Or you’re surprised that organisms grow exponentially after a population crash leaves the culture wide open for repopulation?

Either way…well. Not much to say about that. Good thing too, because work and family are about to vacuum up my free time…

Comment #83656

Posted by BlastfromthePast on March 4, 2006 9:12 AM (e)

BlastfromthePast wrote:
The point is that ‘according to your view’, what wouldn’t ‘grow’ before is now ‘growing’. So WHAT caused it to start ‘growing’? IOW, what ‘triggered’ the growth response? If the ‘unicell’ form has to only be 1.000000001 fitter than the ‘colonial’ form to outcompete it (your numbers), then why all of a sudden does it start to ‘outcompete’ the unicell form? Please explain. Remember that (1) ‘low’ unicell also results in ‘low’ predator, and (2) ‘low’ unicell means 0.1 % of its maximum density. Therefore, if the ‘mutant’ form exists, the ‘unicell’ has only declined in numbers by 10^3, whereas its fitness factor , relative to the colonial form (using your numbers) is 10^8. So the ‘colonial’ form should still be ‘outcompeted’—according to your logic.

Oh dear. The above really makes no sense at all. OK, Population Genetics 101:

Must you be arrogant? You’re convinced that you’re right about all this. Well, let’s see.

Note that this has nothing to do with the actual proportions of X and Y at any given time in the population. Nothing. It just tells you how they’re changing, and how fast. X may start out as .0001% of the population, and if it is consistently fitter than Y—even if it’s only 1.0000000001 times fitter—it will eventually take up 100% of the population and (since population size is finite) Y will go extinct. The smaller the fitness difference, the longer it takes for this to happen, but it’ll still happen. The only way X and Y can stably coexist in the population is if their fitness difference is zero at the steady-state proportions. Of course, if the populations of X and Y change and then stabilize, that means their relative fitness is changing over time.
So trying to compute a “fitness factor” from steady-state population counts, or from the difference between them and the initial counts, or whatever it is you were doing above, is…well, it sure ain’t population genetics. By its very existence a steady state (even with mild fluctuations) implies an average fitness difference of zero (relative fitness of 1).

My dear Anton, you COMPLETELY MISS THE POINT. Do I have—for once—your attention?

All of the above is all well and good. (In fact, it’s perfunctory.) But the whole question here concerns the ‘fitness factors’. We’ve already determined that the ‘unicell’ form is ‘more fit’ than the ‘colonial form’ in nutrient uptake. We’ve determined that the ‘colonial’ form is ‘much more fit’ than the ‘unicell’ form for predation.

With that in mind, you have a culture which, after a ‘grazing down’ by the Ochromonus (5 days), is in a steady-state. BOTH the O. vallecias and the Chlorella are at 0.1 % of their maximum density. The initial density of the Chlorella was 2 x 10^6 cells/ml. For simplicity’s sake, let’s take 0.1 % of the initial density, which is 2 x 10^3 cells/ml.

You’ve assumed all along that a ‘mutation’ occurs. So we have 1 mutated cell. Not 1 mutated cell per ml., but 1 cell in the entire culture. (Remember, now, that you’ve made a big thing about the mutation ‘not being there before’.)

Now, we have a steady-state situation. This means that both the Ochromonus and the Chlorella are going to maintain their levels: the ‘unicells’ keep multiplying and dividing, and the Ochromonus keeps on eating. Excluding chemical induction—which you insist on—then we have a situation in which there is a limited amount of nutrient, for which ONLY the ‘unicell’ and the ‘mutant morph’(= ‘colonial’ form) compete. Now, we’ve ALREADY established that the ‘unicells’ out compete (are ‘more fit’) the ‘colonial’ forms. We also know that there are way more ‘unicell’ forms than ‘colonial’ forms. So “N” (the population size) is greater for the ‘unicells’; and “r” (the fitness factor) is greater for the ‘unicells’. So, tell me, what does Population Genetics 101 tell you is going to happen? The ONLY answer to that is that the ‘unicells’ are going to continue to out compete the ‘colonial form’, keeping it a very low level. So, then, where did the ‘colonial forms’ that were seen (and measured) in the experiment come from?

In fact, your next statement tells us exactly what to expect. Let’s listen:

“Now, let me explain how we’d view this system in terms of fitness. In the absence of the predator, but in strong light, the unicell is slightly fitter than the colony, and this fitness difference is more or less constant w. respect to the populations of the two morphs, because it’s due to things like their respective nutrient absorption efficiency, and that’s not population-size-dependent. Therefore, if you have a culture of the two morphs, the colonies go extinct—“slowly,” because the fitness difference isn’t that big, but inexorably.”

Let me just add: the ‘mutant morph’= ‘colonial form’, doesn’t ‘know’ that the Ochromonus is there. And the presence of the Ochromonus does not add fitness to the ‘colonial form’. Thus the analysis is no different than for the circumstances you just described.

In the presence of the predator, and at most population densities, the colony is fitter than the unicell—but its relative fitness decreases as its proportion in the population increases.

But, of course, as I’ve pointed out above, it is a ‘fitness’ relative to predation, but NOT relative to nutrient uptake.

Anton answers:

Blast responds:

Anton writes: Chlorella isn’t zooplankton.

But it’s closely related.

a) zooplankton is an ecological category, not a phylogenetic taxon, so it’s fairly meaningless to say it’s “related” to anything, and
b) most zooplankton species are way more closely related to us than to Chlorella, being actual metazoan animals.
Again, if you want us to believe you took bio courses…

I’m very happy, Anton, that you think you’re closer to zooplankton than Chlorella is to zooplankton. Chlorella is a phytoplankton. It lives and resides in a similar environment to the zooplankton. If ‘other zooplankton’ show chemical induction, then it is very similar to what is happening here. Ochromonus, a protist, is feeding on the Chlorella just as the other zooplankton were feeding on some other phytoplankton.

Anton responds later on:

Anton first states:

Blast wrote:
It’s not ‘evolution’, since what was there at the end, was there at the beginning.

2) Even if they were, change in the frequencies of pre-existing alleles is still evolution. You know this. You’d call it “micro-evolution,” and it certainly wouldn’t be as interesting a case as what did happen here, but it would be evolution.

Because, for Cthulhu’s sake, you just said “it’s not ‘evolution’, since what was there at the end, was there at the beginning,” and that characterization of evolution is simply wrong. Irrespective of what happened in this experiment, it’s wrong. IDers, YECers, and border collies all know that. So I corrected you.

Well, you’re dealing with me, Anton. Now, tell me, if you have one of those new screwdrivers which can be ‘shifted’ from one kind of tip to another, with ALL the tips in the meanwhile being inside of a canister that is part of the screwdriver, when you switch from one tip to another, has that screwdriver really changed? That is, is it a new ‘species’ of screwdriver each time you change the tip? How do you answer? I think you see the parallel to allelic frequency.

Anton Mates wrote:

Here’s another quote: “We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.” Obviously Boraas is only referring to the replicates where colonies actually happened in the sentence you quote above. There’s a small amount of ambiguity in that particular sentence, but if you actually read the entire paper it’s very clear.
Of course you still haven’t explained why you continue to claim that “70% of cultures have 8-celled mutants” implies “70% of mutations produce 8-celled forms” when you know this is false.

Simple explanation. Here’s a quote from the paper, one that I’ve already posted here. You keep charging me with not having ‘read the paper.’ Well, what can I say. It seems like a case of the ‘pot’ calling the ‘kettle’ black. (Oops.) The quote is from p. 160, the “Significance of this experiment…” section, third sentence.

There’s quite a bit of ‘ambiguity’ between ‘multicell’ and ‘8-cell colonial’ forms. This is a somewhat serious drawback of this paper. They’re not always clear about things. But the two are not the same. And, so, the quote below is very significant when considering chemical induction.
“After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

Anton attempts a response:

Blast writes:
Please explain how the ‘solution’ to the ‘problem of a predator’ is solved in the same way each and every time the experiment is tried? This I’ve got to see.

It isn’t solved the same way, of course, as we see from the initial diversity in colony sizes. A truckload of possible solutions are presented by good ol’ random mutation. 30% of the time no mutation occurs which offers a viable colonial form—kind of what you’d expect since mutations are random—and the unicells win the day. The rest of the time colonies arise, further mutate and diversify, and natural selection, which is obviously non-random, picks the best—which are, predictably, going to be those with 8 or so cells.

Anton blasts Blast:

Blast responds:

Anton writes:
Which isn’t really unexpected, given how you danced around the issue of the “kind” of Helacyton gartleri in an earlier thread, but is rather depressing.

We’re getting a little nasty here, aren’t we? Here’s an answer: a “kind” is a “paradigmatic form”. Okay? As if I really need to explain what it is. Shall I explain what a chair is also? I bet you know one when you see one.

And here we go again—assorted irrelevancies but no answer whatsoever to the question of what “kind” H. gartleri is, whether the “human kind” or some other. I’d ask again, but I lack Lenny’s stamina in asking questions that will never get answers.

I know you don’t like folk expressions; but, as they say, “Ask a stupid question, and you get a stupid answer.”

Anton answers:

Blast writes:
Are you, by any chance, referring to this statement: p.159/160 “The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have been maintained for several months.” My reading of this is that the ‘several months’ refers only to the chemostats kept at steady states. You’re wrong here, and that affects the argument you construct below.

You mean you think the agar and whatever non-cycled liquid cultures lasted longer than that? When there’s no evidence for that, and chemostats are designed for long-term rapid reproduction while agar is not, and Boraas is trying to make a point about how long the colonies bred true for? He actually happened to have some really active colonies on agar for years or something and just forgot to mention it? That makes no sense.

Anton, in biology labs it is a very easy task to culture something from one agar-filled petrie dish to another. You’re hypothesizing. I’m working off what Boraas actually wrote. They “bred true.” That implies lots of generations.

Blast wrote:

On top of that, the average time-to-appearance of the colonial morphs was not 10-20 generations—that was the time it took for the eight-celled morph to dominate the culture after the appearance of colonies.

You disputed this. You were wrong. You didn’t read the paper closely enough. But I’ll get back to what I was referring to when I present proof positive evidence—from the data that Boraas provides—for chemical induction in the next post. Stay tuned.

Anton erupts:

Blast wrote:
There’s a concept used by molecular and evolutionary biologists called the ‘molecular clock’. This ‘clock’ is predicated on a UNIFORM rate of mutation in all organisms. You can fight it out with them. This is just current evolutionary theory.

…and now we know you were lying when you said you took genetics, unless you took it in the ’50s. Every intro genetics student learns about non-uniformity in mutations. Transitions are more common than inversions. Deletions are more common than insertions. Different parts of a chromosome will be more or less vulnerable. Different organisms have vastly different average mutation rates.

Well, Anton, I, indeed, did take Genetics. It was in the early 70’s. And I didn’t do very well. That was because it had to have been one of the most boring, if not the most boring class, I had ever taken before, or since. I’m much more motivated these days, and have several books on my bookshelf. But, please, I know you think you’re omniscient, but you’re not. So, be careful who you call a liar. Thank you.

Anton wrote:
All “molecular clock” models require is the much weaker assumption that the average mutation rate, in certain areas of the genome (usually ones believed not to be under strong selection), in a particular lineage, during a particular timespan, was roughly constant. Sometimes that assumption pans out. Sometimes it doesn’t. But no biologist not currently in a straitjacket believes that every single possible mutation is as likely to occur as any other mutation.
(And of course even if that was the case, as I said before, we have no idea how many mutations correspond to a particular phenotypic change, so some sort of “equal probability of a phenotypic change and its inverse” principle would still be completely unsupportable.)

That’s right. During a ‘particular timespan’, the mutation rate approaches an average. Now why—other than hand-waving—is the ‘reverse’ mutation that much slower than the ‘forward’ one? You say there’s all sorts of ways this ‘mutation’ can come about. Then why aren’t there a whole lot of ways for it to revert? It’s a significant weakness in the argument for mutation.

Thanks for proving my point. The original culture has been at steady-state for twenty years. The colonial cultures, not. Which has had more chance to accumulate mutations, do you think?

I pointed out an error, and this is your response. Based on what you’ve just written, the ‘mutation’ was already there ‘from the beginning,’ a proposition you violently opposed earlier on. You can’t have your cake, and eat it too. Oops. There I go again!

Anton responds:

Blast wrote:
I disagree. The fact that ‘mutation’ is unidirectional has a tremendous bearing on how to interpret these results. As I said before: “what’s good for the goose, is good for the gander.”

Folk proverbs do not substitute for actual well-supported principles of biology. If you have a personal “for any two populations, the probability of a mutation-induced phenotypic change in one is equal to the probability of the reverse change in the other” principle, wonderful. Paint it on a placard and parade it downtown. But you didn’t get that from evolutionary theory.

Whatever ‘evolutionary theory’ is…….It is what it has to be to explain things. They shouldn’t call it ‘evolutionary theory’, they should call it a ‘theory that evolves.’

Comment #83659

Posted by 'Rev Dr' Lenny Flank on March 4, 2006 9:22 AM (e)

Hey Blast, why does Dr Fry (and all the other working scientists you’ve engaged here) think you’re full of crap?

Comment #83680

Posted by k.e. on March 4, 2006 12:28 PM (e)

Well Blasty long time no see.
what have you been doing —arguing with your Quantum Physics teachers ?

So how is the quest for the “Holy Grail” going?
I see you have re-entered the enchanted castle and YOU STILL HAVEN’T asked the question.

Ho Hum…. well at least you made the mistake of saying something true for a change

They shouldn’t call it ‘evolutionary theory’, they should call it a ‘theory that evolves.’

Tuff sh*t old son….. thems the breaks.

You know you could fix this whole thing right now if you wanted.

Look up " rel="external nofollow">Parsifal’s Question.

Comment #83698

Posted by Faidon on March 4, 2006 2:23 PM (e)

Blast wrote:

They shouldn’t call it ‘evolutionary theory’, they should call it a ‘theory that evolves’.

Oh man.

Look, Blast, I’m new here, and I cannot comment on all the things others say about you. However, if this is not just an attempt at humour, and you actually think that is a problem for evolution (or any other scientific theory, for that matter), then forget Genetics: you must have no knowledge of any science whatsoever. Sorry in advance if I’m wrong and it was just an unsuccessful jest, but… Come on.

Comment #83908

Posted by BlastfromthePast on March 5, 2006 7:46 PM (e)

Anton, throughout this discussion, you have steadfastly maintained that what we see in this experiment is no more than some kind of series of mutations taking place in the ‘unicell’ Chlorella population. You have taken the position that these mutations were not there before the predator was introduced. You believe that the 4-cell, 8-cell, 24-cell, 100+-cell ‘colonies’ of Chlorella are no more than different mutations. You also believe, as the authors do, that NS has caused the ‘fittest’ form, the 8-cell ‘colony’ to become dominant.

I have steadfastly maintained from the first time I read of this article that this is a case of chemical induction—knowing nothing of other predator-prey experiments in which chemical induction was shown to be the case.

Rather than letting this go on forever, I now plan on presenting irrefutable evidence—based strictly on the data that Boraas provides—that the colonial form of Chlorella is chemically induced.

I. The first place to start is with the statement, p.160, where it is said: “After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

Phrased another way—a way which should have guided Boraas, et. al.’s thinking—EVERY TIME the experiment was conducted, an 8-celled colony ensued. This bespeaks chemical induction: you introduce the phagotroph, and 8-celled colonies are produced, EACH and EVERY TIME.

This is in contrast to “multicells”—which Boraas doesn’t do a good job of describing, but from what is written and ‘shown’, namely Fig. 1 a.,–that is, colonies greater than 24 cells. “Mulitcells” are found only 70% of the time. So, for 30% of the time, “multicells” have nothing do with the mechanisms at play in this series of experiments.

Again, 8-celled colonies are found 100% of the time.

II. Next, let’s examine what Boraas means by 10-20 generations. It would be wonderful if he would tell us what the doubling time is for the Chlorella. But he doesn’t. But looking at Figure 2a., and by simple calculations based on the percentage increase in the unicell population after it was grazed down by the Ochromonus, the doubling time (time per generation), is a little more than a day. So let’s round down to a day.

Now, let’s address another part of the above statement: “in the presence of the phagotroph.” This implies (and in the discussion this is also apparently what Boraas thought) that the phagotroph excretes some chemical that ‘immediately’ affects the unicell population of Chlorella. But from other similar experiments, it’s been demonstrated that the ‘inducing’ chemical is something that is the product of prey digestion in the predator.

It is fair to assume that for chemical induction to occur, time must be allowed for: (1) the predator to digest the prey. (We don’t know. Let’s assume it takes a day), and (2) a build-up in concentration of the inducer. For both condition (1) and (2) to both occur, we need probably 2-3 days. I think this a conservative, fair assumption.

Now, let’s look at Fig. 2a. We see a peak in the ‘unicell’ at 10 days from introduction of the phagotroph. But just letting your eye move down that time line of 10 days: we also see peaks in the 20, 22, and 25 micrometer range. Boraas states on p. 155-7 that “the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a). The number of cells per colony ranged from four to hundreds (Fig. 1c), and bracketing and masking the flagellate size distribution. (Fig. 2a)”

Using the lower value for generation time, this all occurs at a maximum of 10 generations after the introduction of the phagotroph. But, as I’ve explained above, this number should fairly be reduced to 7 generations (or less). Now, according to your assumptions, a mutation has occurred in ONE of the ‘unicell’ forms which gives rise to the 4-cell, another mutation that gives rise to the 8-cell, another to the 100+-cell, etc. In the description box at the bottom of Fig 2a/b, it is stated that “(t)he majority of Chlorellacells were in colonies with more than 24 cells per colony for the first month of culture.” Notice that 100+-cell ‘colonies’ are ALREADY seen at the 10 day mark. And according to geometric growth, that’s 2^7 times growth starting with one dividing ‘mutant’ cell; in other words, 7 generations worth of growth.

But that is for ONE mutation, resulting in ONE colony. We know that the initial ‘unicell’ Chlorella density is 2 x10^6 cells/ml. It then shrinks to 0.1% of that original density. However, at the 10-day mark, it’s at a value that appears to be almost equal to that initial value: 2 x 10^6 cells/ml. The culture tube volume is said to be ‘volume constant at 500ml.” The most likely situation is that it contains 500 ml. of liquid. But to take a conservative approach here, let’s assume it’s only 250 ml. of liquid in the culture tube. That means there were—at the 10-day mark—5 x 10^8 ‘unicells’ present in the culture tube. Fig 1a. shows the 8-cell size at half that value at the 10-day mark, and the 24-cell value at slightly less. Let’s call the 24-cell value, conservatively, one-fourth of the “unicell” value: that is, 1.25 x 10^8 cells. If we look, now, at Fig 2b, we notice that at the 12 day mark that the 24-cell value is about twice the 100+-cell mark. Assuming a proportionate response between Day 10 and Day 12, that means that the 100+-cell value at the 10-day mark would have been 1/8th of the ‘unicell’: that is, approximately, 6 x 10^7 cells in the culture. But it takes SEVEN generations to produce ONE 100+-cell from ‘one’ mutated cell. So, to back into how many “mutated cells” we need at Day 3 (when the predator’s effect is first felt), we take the 6 x 10^8 and (again, to be conservative) divide by 200 (even though the biomass of a 100+ cell is perhaps not equal to 100 times the ‘unicell’ biomass volume since the ‘colonial’ cells seem smaller in size compared to the ‘free unicells.” (FC in Fig. 1a) Otherwise, we would divide here by 100 [100 ‘unicells’per 100-cell ‘colony’], and not 200), giving a value of 3 x 10^6 cells.

You have assumed the ‘mutations’ have been ‘induced’, hence, to explain these numbers, we need 3 x 10^6 ‘unicells’ “mutating” in such a way that ALL these 3 x 10^6 ‘mutations’ have the same phenotypic effect; viz., 100+-cell ‘colonies’. This is simply IMPOSSIBLE—no matter how many ‘hundreds’ of ways a genome can mutate.

If you want to maintain that the mutation was already there ahead of time (as Pim does), this ‘conservative’ number is only 1/250 th (inverse of the culture tube size assumed here) of the original density of the ‘unicell’. Certainly it would have been seen. Fig 1a was taken 240 days after inoculation, and we see a 24-cell ‘colony’, at a time when the 8-cell was, according to Boraas, dominant, while we were also told that for the first 30 days the 100+-cell ‘colonies’ dominated.

‘Mutation’ of the ‘unicells’ cannot explain the data that is reported.

III. A simple further proof that ‘mutation’ cannot explain what we see reported is the VERY PRESENCE of a 24-cell ‘colony’, let’s notice that that is NOT a ‘power’ of 2. The progression is 2, 4, 8, 16, 32, 64, 128. If we look at Fig 2b, notice that at the 12-day mark there are NO 16-cell ‘colonies’. If a ‘mutant’ is going to produce a 32-cell colony, or a 64, or a 128-cell colony, it MUST pass through the 16-cell stage. There’s no other way possible. Look again at the 24, and 20-cell ‘colonies’—NEITHER of these are multiples of 2. How can it be maintained that something other than an 8-cell ‘colony’ is ‘growing’ when there is no evidence, whatsoever (!!), of the 16-cell stage?

Is this some kind of extravagant claim? Well, let’s take a look at Figure 1. Look at 1a. Doesn’t that look like a 24-cell colony? And doesn’t it look like a cluster of three 8-cell ‘colonies’? Look at 1c. Doesn’t that look like a collection of 8-cell ‘colonies’? And since basic biology says a cell can’t divide in half a multiple number of times and reach a 24-cell stage, the only LOGICAL explanation is that the 24-cell ‘colonies’ are made up of 3 clusters of the 8-cell ‘colonies.’ The 20-cell ‘colonies’ are a combination of two 8-cell ‘colonies’ and a 4-cell ‘colony’.

This can all be simply explained as a change to the mother cell wall coming about via chemical induction.

IV. Lastly, let’s take another look at Fig 2b. Notice that around Day 45-50, the 8-cell ‘colonies’ have the ‘dominating’ the “biomass volume”. But also notice that there are “biomass volume” peaks at the 20-cell and 24-cell ‘colonies’. And remember Fig 1a. There we see a 24-cell ‘colony’ after 240 days after inoculation, a ‘colony’ that clearly looks like three clustered 8-cell ‘colonies.’

To sum up:

1.) In EVERY replicate of this experiment, the 8-cell ‘colony’ is observed and becomes permanent.

2.) The presence of 100+-cell ‘colonies’ cannot be explained via the ‘mutation’ of the Chlorella ‘unicells’ either through ‘induction’ by the presence of a predator, or through these ‘mutations’ being present in the culture before the experiment began.

3.) Photographic evidence strongly suggests that clusters larger than the 8-cell ‘colonies’ are the product of a clustering of 8-cell ‘colonies’. The persistent presence of 24-cell ‘colonies’, which defies the geometric progression of cell division, buttresses this observation.

This not only rules out RM+NS, it paves the way to proving a chemical induction scenario for what is observed.

That scenario goes like this:

If the presence of the predator-prey by-product is the ‘trigger’ for a change in thickness/stickiness of the ‘mother cell wall’ of the Chlorella, that ‘trigger’ would likely have come about in Day 3. This ‘signal’ affects all ‘unicells’ that will go on to become ‘mother cells’. The ones that do not become ‘mother cells’ are ‘grazed down’ and stay in a steady-state with the Ochromonus. The ‘mother cells’ that respond begin to divide. Normally, the ‘mother cells’ contain 2-16 cells. With chemical induction having taken place, some of the mother cells continue to divide and grow, reaching the 16-cell count wherein it ‘bursts’ in half. But now, since chemical induction has occurred, the membrane ‘sticks’ to the cells, forming 8-cell ‘colonies’. It’s possible that some ‘mother cells’ burst at the 8-cell stage, thus forming 4-cell ‘colonies.’ The remaining colony cell numbers, in particular the 24-cell ‘colony’, come about by 8-cell ‘colonies’ ‘sticking’ together. In the transient period, ‘stickiness’ prevails, and large-celled ‘colonies’ (over 100 cells) occur. [N.B. this ‘transient’ period could be—and I would go so far as to say, probably is—attributable to this experiment being performed in a ‘culture tube’, rather in a natural planktonic environment.] In the end, the 8-cell ‘colony’ predominates in EVERY experiment run.

One important final word: the clear indicator between the ‘unicell’ morph and the ‘colonial’ morph is the presence of ‘empty’ ‘mother cells.’ It is noted that in the ‘unicell’ culture, empty mother cells could be seen, whereas when the ‘colonial’ form is present, NO empty mother cells are detected. This is easily explained—almost predicted—from my proposed mechanism in the above paragraph.

That is why it is of paramount importance to know what happened in the chemostat when the phagotroph was removed and the ‘unicellular’ form and the ‘colonial’ form were present together. In the absence of the predator-prey chemical inducer, AND, in the presence of a normal, almost background, signal that the ‘unicellular’ forms produce, one would expect that the ‘mother cell walls’ would be affected, they would return to their normal condition, AND…… ‘empty’ ‘mother cell walls’ would begin to be seen.

Isn’t it interesting that when it comes to this absolutely important information we’re simply told, “In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the LIGHT, the multicellular form was slowly displaced by unicells (data not shown).”

As to Boraas’ principle reason for claiming that ‘induction’ has not occurred, I think he has made two mistakes. First, he assumes that the ‘induction’ begins ‘immediately’ with the introduction of the phagotroph. Other experiments demonstrate otherwise. It is very likely that the ‘signal’ for the 8-cells comes when the ‘unicells’ have been ‘grazed down’ to its steady-state density. This is 5-days after the phagotroph is introduced. Second, he assumes that the ‘induction’ is to the ‘unicells’ directly; but, more probably, it is to the ‘mother cell wall.’ The effect of that ‘induction’ is not seen until the first affect ‘mother cells’ burst. This is at a cell size of 16; that is, 2^4; in other words, after 4 generations. How long does it take for four generations of Chlorella to form? About 4-5 days. Under the proposed chemical induction scenario, one would expect the “8-cell colonies” to appear 9-10 day after the phagotroph is introduced—which is EXACTLY what is seen. Similarly, to ‘return’ to normal behavior where the phagotroph is absent would be, at a MINIMUM, around 4-5 days. Is that what Boraas means by “slowly displaced”? Too bad there’s “NO DATA SHOWN”.

In conclusion, there is no question that what we’re seeing in the Chlorella is some kind of chemical induction, likely to the ‘mother cell wall.’ RM+NS cannot explain the data that is presented here. Photographic evidence supports this conclusion.

This paper passed peer-review. PTers/Darwinists make a big deal of peer-review. What this paper demonstrates is that the Darwinist world-view blinds scientists—both the authors and the reviewers—from taking a critical view of data.

As far as I’m concerned, the discussion of this paper, and the chemical induction vs. RM+NS interpretation of this paper, are concluded. The conclusions I’ve made above are clear-cut and irrefutable.

Case Closed.

Comment #83909

Posted by PvM on March 5, 2006 8:00 PM (e)

Just because Blastfromthepast hopes that the issue is closed does not make it so. In fact, any time someone makes the claim of irrefutible, my baloney detector overloads.

First issue, did the multicellular form arise in all experiments?

Also there is a 5th reason why induction does not seem to be a very good thesis. In only 70% of the replicants did the experimenters see a repeat of multicellularity. This is understandable from a selection perspective but not from an induction perspective.

The paper states “We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.”

Blast may have misinterpreted the statement

After about 10±20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.

In about 70% of the replicates, a multicellular form arose, when such a form arose, in all experiments they settled on 8 cells.

This does not bode well for ‘irrefutable’ now does it.

Comment #83910

Posted by Sir_Toejam on March 5, 2006 8:02 PM (e)

As far as I’m concerned, the discussion of this paper, and the chemical induction vs. RM+NS interpretation of this paper, are concluded.

lol.

Also sprach Zarathustra.

Comment #83923

Posted by Faidon on March 5, 2006 8:46 PM (e)

You know, call me naiive, but until now I had this hope Blast might actually be serious and have some genuine views to uphold, however wrong- not just some clueless geek trying to gain impressions. Oh well.

Comment #83937

Posted by BlastfromthePast on March 5, 2006 9:34 PM (e)

PvM wrote:

Blast may have misinterpreted the statement

After about 10±20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.

In about 70% of the replicates, a multicellular form arose, when such a form arose, in all experiments they settled on 8 cells.

This does not bode well for ‘irrefutable’ now does it.

Pim, you’re a gentleman. But I think it might be you who is mistaken here.

First, let’s note that this article is flawed in its failure to explain the terms they use properly, and in not giving us information that is at times pertinent, and at others, essential.

I direct your attention to Fig. 1. In Fig 1a, we have a 24-cell ‘colony’ that is called exactly that–a ‘colony.’ It’s not called a “multicell” Chlorella. And, let’s note, it is NOT 8-celled. Now look at Fig 1c. Here we have a grouping of unicell Chlorella that numbers probably in the hundreds. What do they call it? Here’s their words: “A large, multicellular Chlorella colony subjectd to 8 days of grazing by Ochromonus.” There you have it: ‘multicells’ are very large ‘colonies’.

In the section where they talk about the “70% of the replicates”, they also talk about a “budding process” (which, characteristically, they do a poor job of describing).

Since you think it’s a ‘fifth reason’ that this isn’t ‘induction’ that we’re witnessing, then why didn’t they conclude the same thing and include it in their paper?

Because ‘multicelluarity’ in ‘70% of the replicates’, and the presence of 8-celled ‘colonies’ in ALL replicates are two different matters.

Look at what they said about it: “In 70% of the replicates a multicellular form arose….” They didn’t say ‘colony’, whereas in the first quote they do–without mention of ‘multicelluarity.’

It’s not me that is confused. But it would have behooved the authors to have been more clear about ‘multicells’ versus ‘colonies’, and elaborated more about this ‘budding’ process. It would have helped us all.

Comment #83939

Posted by BlastfromthePast on March 5, 2006 9:43 PM (e)

Faidon wrote:

You know, call me naiive, but until now I had this hope Blast might actually be serious and have some genuine views to uphold, however wrong- not just some clueless geek trying to gain impressions. Oh well.

Oh, the faint-hearted. If you’re so easily influenced by the high-sounding words of the so-called experts, then I don’t have much hope for you being able to ferret out who’s right and who’s wrong here.

Follow their arguments. I’m only going to respond to an argument that comes close to making sense. I’m not going to waste my time on the silly ones.

Pim’s response–and I respect him–did not go to the heart of my argument. He took an easy swipe at me. I’ve answered cogently. Let’s see what comes next.

Comment #83940

Posted by PvM on March 5, 2006 9:45 PM (e)

First, let’s note that this article is flawed in its failure to explain the terms they use properly, and in not giving us information that is at times pertinent, and at others, essential

So your interpretation is not that irrefutable after all?

Since you think it’s a ‘fifth reason’ that this isn’t ‘induction’ that we’re witnessing, then why didn’t they conclude the same thing and include it in their paper?

Because the four reasons given were quite convincing by themselves?

In an experimental predator-prey system, predation by the phagotrophic predator Ochromonas vallescia reproducibly selected for multicellularity within a population of the unicellular alga Chlorella vulgaris (Boraas et al., 1998).
Whereas some predators secrete pheromones that can induce colony formation in their prey, the transition to multicellularity in this example was heritable and stable in the absence of the predator. The rapid evolution of multicellularity demonstrates a latent and normally untapped genetic potential within populations of C. vulgaris.
Furthermore, it lends credence to the idea that predation may have selected for fixation of multicellularity in the unicellular progenitors of animals

And now for some reading comprehension

“A large, multicellular Chlorella colony subjectd to 8 days of grazing by Ochromonus.” There you have it: ‘multicells’ are very large ‘colonies’.

Huh… a large multicellular colony is hardly the same as multicells. Geez
Cheers my friend. Good luck.

Comment #83941

Posted by BlastfromthePast on March 5, 2006 9:45 PM (e)

Sir Toejam wrote:

Also sprach Zarathustra.

I sense the thunderbolts have blinded you, but did you hear the thunderclaps?

Comment #83942

Posted by BlastfromthePast on March 5, 2006 9:58 PM (e)

PvM wrote:

Huh… a large multicellular colony is hardly the same as multicells. Geez
Cheers my friend. Good luck.

And now for some reading comprehension:

p. 157. “Colonies had variable morphologies, even during the steady-state phase, but the majority were roughly spherical, usually with eight (but occasionally four) cells per colony.” That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4). Anything else is a ‘multicell.’ And, yes, a “multicell” is a large–a very large (LOOK AT the PICTURE)–‘colony’, which, apparently, reproduces differently than the ‘true’ 8-celled ‘colonies’; i.e., they ‘bud’.

Tell me, Pim, in all honesty, wouldn’t you have appreciated them giving us a little more detail on this?

Comment #83943

Posted by PvM on March 5, 2006 10:00 PM (e)

Tell me, Pim, in all honesty, wouldn’t you have appreciated them giving us a little more detail on this?

Are you sure you are not projecting here? You claimed irrefutable… Care to rephrase?

Comment #83948

Posted by PvM on March 5, 2006 10:54 PM (e)

So let’s accept BlastFromthePast’s argument that the reponse was induced chemically. What does this mean for Darwinian theory?
While initially epigenetically controlled, the stability of the 8 cell variant shows that selection and variation eventually led to a significant novelty namely multicellularity.
Evolution works in mysterious ways :-)

How does ID explain this?

Realize that the step from single to multicellularity (coloniality) was the first step. Next step is cells taking on specialized roles. Science is slowly unraveling these mysteries.

ID seems to remain well, a bit vacuous.

Comment #83951

Posted by BlastfromthePast on March 6, 2006 12:22 AM (e)

PvM wrote:

You claimed irrefutable… Care to rephrase?

I’m rather certain I’ve interpreted Boraas correctly. But if his presentation had been better, then I wouldn’t have had to work so hard to unravel the perplexities he left for us.

Comment #83952

Posted by PvM on March 6, 2006 12:29 AM (e)

I’m rather certain I’ve interpreted Boraas correctly. But if his presentation had been better, then I wouldn’t have had to work so hard to unravel the perplexities he left for us.

Poor Blast… Hard work never has hurt anyone but to claim irrefutable evidence when you yourself consider Boraas’s work to be less than clear seems rather … well… you know.

You made the claim. now you seem to regret it :-)

Comment #83953

Posted by Sir_Toejam on March 6, 2006 12:35 AM (e)

I’m only going to respond to an argument that comes close to making sense. I’m not going to waste my time on the silly ones.

hey, stop stealing our lines.

Comment #83956

Posted by Sir_Toejam on March 6, 2006 12:51 AM (e)

…but did you hear the thunderclaps?

no, but did you hear that God is dead?

Comment #83957

Posted by PvM on March 6, 2006 12:53 AM (e)

Pim’s response—and I respect him—did not go to the heart of my argument. He took an easy swipe at me. I’ve answered cogently. Let’s see what comes next.

I took a swipe at your irrefutable claim and showed that there is sufficient uncertainty that such a claim is unwise.

The strongest argument against induction is that the 8 cell structures bred true and that they were maintained even when the predator was absent.

That by itself makes an induction argument quite shakey.

Blast wrote:

hat’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4). Anything else is a ‘multicell.’ And, yes, a “multicell” is a large—a very large (LOOK AT the PICTURE)—‘colony’, which, apparently, reproduces differently than the ‘true’ 8-celled ‘colonies’; i.e., they ‘bud’.

And yet colony is used to refer to sizes ranging from 2 and greater than 100.

The majority of Chlorella cells were in colonies with more than 24 cells per
colony for the first month of culture.

and

Colony growth was a ‘budding’ process, based on visual observations. Individual cells of the colony grew in size while dividing into daughter cells; the new colony then separated from the original colony by tearing or breaking the original mother cell wall. We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.

Contrary to Blast’s claims colonies are not limited to size 4 or 8.

Comment #84206

Posted by BlastfromthePast on March 6, 2006 6:40 PM (e)

PvM wrote:

I took a swipe at your irrefutable claim and showed that there is sufficient uncertainty that such a claim is unwise.

The strongest argument against induction is that the 8 cell structures bred true and that they were maintained even when the predator was absent.

That by itself makes an induction argument quite shakey.

You’re taking a ‘swipe’ at what’s incidental.

The authors mention 4 reasons for dismissing the chemical induction ‘alternative’ hypothesis. This ‘supposed’ 70% replication of ‘multicells’ is not one of them.

As to their ‘breeding true’, if your read my long post carefully, that issue is addressed. The article states clearly that when you mix the unicells with the ‘colonies’ in the absence of the phagotroph, the ‘colonies’ disappear. They say that they ‘slowly dissolve’. I address that very point in the post.

Unfortunately, and somewhat mysteriously, they simply put, “data not shown”. (Notice that they don’t say, “data not available”. Was there a nefarious reason for not including this data?)

Finally, here is what the article states.

p.157 “Colonies had variable morphhologies even during the steady-state phase, but the majority were roughly spherical, usually with eight (but occasionally four) cells per colony.

4-cell Chlorella are phototrophs. 8-cell Chlorella are phototrophs. Unicell Chlorella are phototrophs. All are phototrophs.

p.160 “The Chlorella had maintained the normal unicellular body shape for thousands of generations in the same laboratory culture conditions. After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

They state that the 8-cell ‘colony’ became the ‘dominant’ phototroph in ALL replicates. ALL replicates.

Case closed.

Comment #84220

Posted by Russell on March 6, 2006 6:56 PM (e)

I don’t have the patience to read all the way through what looks like yet another tedious grasping at straws by Mr. Blast. So forgive me if this has already been asked and answered.

But if Blast favors this “induction” hypothesis, and looks to my cursory examination to be determined to shoehorn the evidence into that explanation, what tests does he propose that could potentially disprove it? (You know, that “falsifiability” thing.)

Comment #84226

Posted by BWE on March 6, 2006 7:09 PM (e)

or, for that matter, “prove” that it is the best hypothesis?

Ha ha.

Comment #84248

Posted by Popper's Ghost on March 6, 2006 8:02 PM (e)

p. 157. “Colonies had variable morphologies, even during the steady-state phase, but the majority were roughly spherical, usually with eight (but occasionally four) cells per colony.” That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4). Anything else is a ‘multicell.’ And, yes, a “multicell” is a large—a very large (LOOK AT the PICTURE)—‘colony’, which, apparently, reproduces differently than the ‘true’ 8-celled ‘colonies’; i.e., they ‘bud’.

Why did Blast start his highlight just after the word “usually”? Does it possibly have anything to do with being, um, DISHONEST?

Comment #84250

Posted by Popper's Ghost on March 6, 2006 8:07 PM (e)

P.S. This is obviously (to any honest person) not a definition of “colony”, but rather a description of the colonies that were observed. “colony” is presumed to have its usual meaning.

Comment #84303

Posted by Anton Mates on March 6, 2006 10:05 PM (e)

Popper's Ghost wrote:

Why did Blast start his highlight just after the word “usually”? Does it possibly have anything to do with being, um, DISHONEST?

I suspect it’s the same reason as why he quoted:

p.160 “The Chlorella had maintained the normal unicellular body shape for thousands of generations in the same laboratory culture conditions. After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.

and failed to highlight the “After about 10-20 generations in the presence of the phototroph.” Since that part clearly indicates that if there weren’t any eight-celled colonies to be in the presence of the phagotroph, then they didn’t become the dominant phototroph. And so this doesn’t conflict with the

We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.

statement at all.

And yes, dishonesty is the most parsimonious hypothesis, but we know how he feels about parsimony. Perhaps we should hypothesize a complex genetically-coded, front-loaded algorithm that only looks like dishonesty.

I was going to continue pointing out errors from where I left off once I have more free time tomorrow, but at this point perhaps it’s just an exercise in the obvious.

Comment #84325

Posted by PvM on March 6, 2006 11:17 PM (e)

Nice analysis Anton. Indeed, the two statements do not conflict *if* read correctly.

Comment #84358

Posted by W. Kevin Vicklund on March 7, 2006 12:12 AM (e)

But if Blast favors this “induction” hypothesis, and looks to my cursory examination to be determined to shoehorn the evidence into that explanation, what tests does he propose that could potentially disprove it?

Obviously, I’m not Blast (if nothing else, because I’m actually responding sincerely and honestly to this question), but the use of permeable membranes could falsify the induction hypothesis. Establish two populations of Chlorella on both sides of a permeable membrane, add the predator to only one side, and see if the colonial form arises on both sides or just the side with the predator (for those experiments in which colonial forms actually arise). That would test for A and B, if I remember the argument correctly.

To test for hypothetical inducer C, separate a population of colonial forms from a population of unicellular forms with a permeable membrane. Watch and see if the colonies become unicellular. Another test for C is to add a genetic marker, say a gene that codes for fluorescence, to the colonial genome (ie, replicate the original experiment with Chlorella with the marker), then add normal, markerless unicellular forms and let the colonials wash out. This will tell you if the colonials are returning to a unicellular state (inducement) or are being selected against by observing whether the final result contains any unicellular forms with the marker.

Comment #84378

Posted by Sir_Toejam on March 7, 2006 12:56 AM (e)

but the use of permeable membranes could falsify the induction hypothesis

and if blast were truly serious about his qestions, this would be a very easy thing to do. cheap experiment to set up and run.

of course, he won’t learn much about the methods or analysis he needs in his quantum mechanics course.

Comment #84454

Posted by Popper's Ghost on March 7, 2006 6:01 AM (e)

P.P.S.

p. 157. “Colonies had variable morphologies, even during the steady-state phase, but the majority were roughly spherical, usually with eight (but occasionally four) cells per colony.” That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4).

This is really very illuminating. Let’s pick a random entry from google scholar … ok:

http://www.csa.com/partners/viewrecord.php?reque…

“Colonies had a density of 4.2/km super(2) but exhibited considerable spatial clumping.”

That’s their definition for a ‘colony’: A colony has a density of 4.2/km^2 … and exhibits considerable spatial clumping.

Wow, I hadn’t realized that ‘colony’ could be defined in so many – and such specific – ways.

Comment #84514

Posted by BlastfromthePast on March 7, 2006 10:47 AM (e)

W. Kevin Vicklund wrote:

Obviously, I’m not Blast (if nothing else, because I’m actually responding sincerely and honestly to this question), but the use of permeable membranes could falsify the induction hypothesis. Establish two populations of Chlorella on both sides of a permeable membrane, add the predator to only one side, and see if the colonial form arises on both sides or just the side with the predator (for those experiments in which colonial forms actually arise). That would test for A and B, if I remember the argument correctly.

To you, W., and all the others who have taken potshots, I think ad hominem arguments are just wonderful examples of high-level science. Keep it up.

Now, as to the quote above, they’ve done experiments with different zooplankton in which chemical induction is involved where they have shown that physical contact by the predator/prey is necessary. So what you suggest may not be proof positive that induction takes place or not.

As I said before, if in the instance when there was no phagotroph in the ‘unicell’ and ‘colony’ mixture no ‘empty mother cell membranes’ were seen, I suspect that might rule out chemical induction.

Comment #84516

Posted by k.e. on March 7, 2006 10:48 AM (e)

Gee Blast wedged again what’s your average now… twice a month ?

By induction you seem to have some impermeable and false beliefs that if not changed will lead to an even more tenuous grasp on reality….. if that were possible.

At least you are not projecting your completely useless religious beliefs as science facts, you know the one about “for 150 years now creationist’s have been denying evolution…blah blah blah” have you given those up ?
Good for you if you have….uh oh …wait a minute…. induction? hahahahahahaha.

Yes the easily debunked Dembski/JAD “if we can only come up with a way of describing evolution without motioning anything about it and/or if we have to…. use a negative or counter argument, that is ……wait for it…..(lights, trumpets, clarions)….TADA…. deduction and thus irrefutable god er the Karl Lagerfield/Christen Dior of nature exists NOW MORE FASHIONABLE, ready to wear Creationism.
PLUS THE DESIGNER HAS A PhD. heck he has two of them. One in basic plant’s and animals and the other in his SPECIAL SUBJECT HomoSapiens.
Roll up roll up get your designer books here. Our motto is “We may have designs on your money but hey YOU WILL FEEL BETTER !

No this is not your dusty old Sunday school version of the pre Star Wars version of an unshaven Alan Greenspan in drag doing god but the new Hip cool (and white male sensitive new age redneck) version of god …..oh did I mention he was intelligent ?
Well maybe but only if you count a basic good education as a mark of intelligence heck some of those guys have one or two Ph.D’s

Let us know how you are going to fix Quantum Mechanics the same way you have irrefutably smirk fixed biology.
Good luck there are even more loonies, crack pots and pseudo scientists on that circuit but there are a few who have really, really, really sorted it all out have you heard of Dr Quantum ? he has a PhD. and met Werner Heisenberg really and he has 11 books. WoW Blast when are you going to give us your pearls in a book ?

Comment #84521

Posted by k.e. on March 7, 2006 10:55 AM (e)

motioning mentioning ….stupid spell checker

Comment #84523

Posted by BlastfromthePast on March 7, 2006 11:01 AM (e)

W.Kevin Vicklund wrote:

To test for hypothetical inducer C, separate a population of colonial forms from a population of unicellular forms with a permeable membrane. Watch and see if the colonies become unicellular. Another test for C is to add a genetic marker, say a gene that codes for fluorescence, to the colonial genome (ie, replicate the original experiment with Chlorella with the marker), then add normal, markerless unicellular forms and let the colonials wash out. This will tell you if the colonials are returning to a unicellular state (inducement) or are being selected against by observing whether the final result contains any unicellular forms with the marker.

Sorry, Kevin, I hadn’t read this part when I responded the first time.

Both these experiments seem as though they would work. The first seems relatively easy to do. But, like I said in the post before, the mere absence of ‘empty mother cell walls’ would be enough to give you a good idea of induction or no-induction. Unfortunately (or worse), we’re told: “data not shown”, for that portion of the experiment.

Comment #84563

Posted by PvM on March 7, 2006 12:14 PM (e)

To you, W., and all the others who have taken potshots, I think ad hominem arguments are just wonderful examples of high-level science. Keep it up.

Potshots? Or showing how your ‘arguments’ are refutable after all? Come on Blast, if you cannot even stand up and defend your ‘irrefutable’ claims then perhaps science is too hot for you.

Comment #84567

Posted by PvM on March 7, 2006 12:23 PM (e)

Unfortunately, and somewhat mysteriously, they simply put, “data not shown”. (Notice that they don’t say, “data not available”. Was there a nefarious reason for not including this data?)

Why is Blast suggesting that there may be a ‘nefarious reason’ for not including the data? What is so mysterious about ‘not showing all the data’?

Typically an experiment generates far more data than can be shown in a paper. Some papers allow for supplements to be published online.

So far let’s see how well Blast is doing?

To sum up:

1.) In EVERY replicate of this experiment, the 8-cell ‘colony’ is observed and becomes permanent.

2.) The presence of 100+-cell ‘colonies’ cannot be explained via the ‘mutation’ of the Chlorella ‘unicells’ either through ‘induction’ by the presence of a predator, or through these ‘mutations’ being present in the culture before the experiment began.

3.) Photographic evidence strongly suggests that clusters larger than the 8-cell ‘colonies’ are the product of a clustering of 8-cell ‘colonies’. The persistent presence of 24-cell ‘colonies’, which defies the geometric progression of cell division, buttresses this observation.

1. has been shown to be based on an incorrect reading of the paper.

Lets see what we can do with 2 and 3

Comment #84580

Posted by pvm on March 7, 2006 12:45 PM (e)

In continuous cultures with the predator, the rapid appearance of very large multicellular Chlorella (Fig. 1c) apparently resulted from incomplete division: an initial loss of the mechanism for separating successive generations.

So here we have the mechanism. Incomplete division because of the loss of the mechanism for separating successive generations.

The most probable initial mechanism for colony formation, adhesion of the daughter cells to the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies (Fig. 1d) and the absence of cast-o€ mother cell walls in cultures dominated by colonial morphs (personal observation). Incomplete cell division has also been proposed as a mechanism for selection of elongated bacteria in the presence of protozoan
predation (Shikano et al., 1990; Gillott et al., 1993).
Two potential mechanisms for reducing colony size were suggested from electron micrographs of multicellular Chlorella. First, the original mother cell wall became increasingly fragile in multicells. The enclosing membrane of colonies from cultures 20-100 days old had a ‘ropy’ appearance (Fig. 1a). Such ‘ropes’ could form if the mother cell wall split and curled on itself, unlike wild-type cell walls. As the daughter cells grew, the ‘ropy’ form may have broken more readily than the earlier ‘sheet’ form of the mother cell wall (Fig. 1d). Secondly, colonial cells shared cell walls (Fig. 1f: two cells, from a culture 540 days old). One of the cells (Fig. 1f) was dividing, implying
division may not have been synchronous within colonies. As the cells grew and their radii increased, the cell walls would slowly tear apart, with separation occurring at some critical radius

Comment #84621

Posted by BlastfromthePast on March 7, 2006 1:38 PM (e)

All of you keep harping on this 70% of multicells thing.

A clear reading of the text demonstrates, unequivocably, that the authors refer, at times, to ‘colonies’ and to ‘multicells’, as well as to ‘multicell colonies’ (Fig 1c). If they didn’t want to distinguish between ‘multicells’ and ‘colonies’, then why introduce BOTH terms? Why didn’t they just talk about ‘colonies’, or just talk about ‘multicells’? The only conceivable reason is that they are making some kind of distinction.

Thus, when they say that ‘multicells’ appeared in 70% of the replicates, and then say that an 8-cell colony became the dominant phototroph in ALL replicates, why is it you infer that the 8-celled colonies only appeared in 70% of the replicates? How does this follow?

Fig. 1a shows an Ochromonus, and what appears to be a 24-cell Chlorella form which they label a “Chlorella colony”. That also would be a phototroph–still there after 240 days after inocculation with the Ochromonus. It isn’t called a ‘multicell’. Again, in all replicates the 8-celled became the dominant phototroph. After 240 days, there are 1-cell, 4-cell, 8-cell and 24-cell phototrophs present. And the 8-cell is dominant. The language is clear. So the onus is on you to prove that when the authors were talking about ‘multicells’, they really meant ‘colonies’.

Prescinding from the above argument, all of you are argue that the fact (which is clearly in dispute if it is to mean 8-celled colonies as well) that the Chlorella only became ‘multicell’ in 70% of the replicates is ‘proof-positive’ that this isn’t ‘chemical induction.’

Well, if it is ‘proof-positive’ that what we see in the experiment isn’t chemical induction, then why don’t the authors state this as the very FIRST reason to discount what they call the ‘alternative hypothesis’ of chemical induction?

In fact, they don’t even cite it as a reason AT ALL to discount the chemical induction idea.

You’re all indulging in a strawman argument since you cannot refute the logic I use in positively refuting the idea that the experimental data presented in the paper represents RM+NS. Why don’t you admit defeat?

Comment #84624

Posted by k.e. on March 7, 2006 1:47 PM (e)

Blasty I hate to say this about another human but you are Pathologically beyond reason.
EVERY SINGLE argument you have started has been demolished
WHY IS THAT ?
You need to do some real soul searching, start with your own beliefs and question their effect on your motivation and ask WHY it is you keep getting every view of the world you construct in your mind ….inside out and backwards.

Comment #84638

Posted by Popper's Ghost on March 7, 2006 2:09 PM (e)

I think ad hominem arguments are just wonderful examples of high-level science. Keep it up.

Indeed, we will keep up pointing out your dishonesty – which is essential to high-level science. For the integrity of science to be maintained, fraud and charlatanry cannot be tolerated.

Comment #84703

Posted by BlastfromthePast on March 7, 2006 4:05 PM (e)

Indeed, we will keep up pointing out your dishonesty — which is essential to high-level science.

We’re the authors of this paper being ‘honest’ when they left out critical data? Are you attacking the wrong person?

Comment #84705

Posted by Sir_Toejam on March 7, 2006 4:09 PM (e)

We’re the authors of this paper being ‘honest’ when they left out critical data

since, as has been pointed out to you clearly more than once… they did NOT, the attacks directed towards you are spot on….and you’re still a buffoon.

Comment #84712

Posted by Steviepinhead on March 7, 2006 4:30 PM (e)

It pays to recall underlying motivations.

What’s really got Blast’s knickers in a bunch is the ramifications of this interesting experiment: an ecological rationale for single-celled eukaryotes to adopt multicellularity (Natural Selection); and normally single-celled eukaryotes with sufficient variability to accomodate to this environmental stress by, literally, sticking together (Random Mutation).

In short, a feasible and detailed scenario for a key step in the “goo to you” evolutionary sequence. One that shivers the deepest foundations of Blast’s world-view; one that, from Blast’s perspective, threatens his very soul.

He simply cannot abide this result (any more than Paley’s Ectoplasmic Essence could abide the sea-to-land transition of tetrapods, another key step in the same evolutionary sequence, and one which is also coming into ever-sharper focus, and becoming ever more difficult to deny…).

Shocked to his core by this gut-punch, Blast has only two choices, one of which–reformulate his entire approach to reality–Blast views as equivalent to the the termination of his personality. He is left with no choice, therefore, but to critique, carp, and quibble until the immediate crisis is past.

Anything, in other words, but face up to the immediate implications of the evidence.

Comment #84758

Posted by BlastfromthePast on March 7, 2006 6:03 PM (e)

Steviepinhead wrote:

Shocked to his core by this gut-punch, Blast has only two choices, one of which—reformulate his entire approach to reality—Blast views as equivalent to the the termination of his personality. He is left with no choice, therefore, but to critique, carp, and quibble until the immediate crisis is past.

Stevie, there’s a word for all this, you know. That word is ‘projection’.

To any lurkers out there, the Darwinists are stymied by my arguments, and instead of rebutting the arguments, they spread venom. All of this so as to create the impression of: “How can all these people be wrong, and this other guy (who they call all kinds of names) be right.” That’s their way of “winning” arguments. Fascists would be proud.

Comment #84763

Posted by Sir_Toejam on March 7, 2006 6:14 PM (e)

like we keep saying, idiot, if you’re so sure you have something to contribute, why don’t you?

rather than suffer the slings and arrows of outrageous fortune, why not actually participate in the real world?

go do some friggin’ research, or shut yer yap, doofus.

oh, that’s right, you’d prefer to take a class in quantum mechanics instead.

you’re one pathetic waste of space, much like all the rest of the IDiots out there who similarly choose to spend all their time whining rather than doing research.

Since you think yourself Zarathustra, why don’t you go and prove us all wrong, eh?

Comment #84765

Posted by BlastfromthePast on March 7, 2006 6:19 PM (e)

Sir Toejam wrote:

go do some friggin’ research, or shut yer yap, doofus.

I once had an opportunity to do research. And guess what? The PhD. I was working for wanted to fudge our results on a grant application.

Yes, we must have ‘honesty’ to do ‘high-level science.’ And then they said, “Data not shown.”

Comment #84767

Posted by Sir_Toejam on March 7, 2006 6:22 PM (e)

I once had an opportunity to do research. And guess what? The PhD. I was working for wanted to fudge our results on a grant application.

ahh, so that’s it eh?

past injustices preventing you from living your life?

your old major prof quashing every attempt you make to publish articles eh?

or is it just more whining?

come on now, face your demons, boy.

or just keep shaking your fist harder.

Comment #84770

Posted by PvM on March 7, 2006 6:25 PM (e)

Oh man… We point out how Blast butchered the interpretation of the paper and now he uses desperate arguments to save whatever little is left.

All of you keep harping on this 70% of multicells thing.

A clear reading of the text demonstrates, unequivocably, that the authors refer, at times, to ‘colonies’ and to ‘multicells’, as well as to ‘multicell colonies’ (Fig 1c). If they didn’t want to distinguish between ‘multicells’ and ‘colonies’, then why introduce BOTH terms? Why didn’t they just talk about ‘colonies’, or just talk about ‘multicells’? The only conceivable reason is that they are making some kind of distinction.

So you say…

Thus, when they say that ‘multicells’ appeared in 70% of the replicates, and then say that an 8-cell colony became the dominant phototroph in ALL replicates, why is it you infer that the 8-celled colonies only appeared in 70% of the replicates? How does this follow?

Simple careful reading of the paper. When multicells appear, the 8-cell colony became on all cases the dominant phototroph.

Prescinding from the above argument, all of you are argue that the fact (which is clearly in dispute if it is to mean 8-celled colonies as well) that the Chlorella only became ‘multicell’ in 70% of the replicates is ‘proof-positive’ that this isn’t ‘chemical induction.’

Well, if it is ‘proof-positive’ that what we see in the experiment isn’t chemical induction, then why don’t the authors state this as the very FIRST reason to discount what they call the ‘alternative hypothesis’ of chemical induction?

So now the argument is that since the authors did not mention it, therefor the conclusion we have drawn must be wrong. Following this logic, the fact that authors mentioned that they rejected the induction hypothesis means that Blast’s conclusion must be wrong. After all, fair is fair.

In fact, they don’t even cite it as a reason AT ALL to discount the chemical induction idea.

You’re all indulging in a strawman argument since you cannot refute the logic I use in positively refuting the idea that the experimental data presented in the paper represents RM+NS. Why don’t you admit defeat?

Yes, why don’t you Blast. So far you have been not only shown to be wrong about irrefutable but your assertions that the authors somehow omitted critical data is both an insult to these authors as well as to common logic.

Blast wrote:

We’re the authors of this paper being ‘honest’ when they left out critical data? Are you attacking the wrong person?

So it is to Blast to show that the authors were somehow dishonest and that critical data was omitted.

While the first of Blast’s three ‘arguments’ has been solidly rebutted as a misreading on his part, the second and third argument seem to fare not much better. More in a later posting. Hint: The concentration of chlorella dropped significantly during the first 5 days, in other words, the genetic multicell variants increased in relative concentration.

Comment #84795

Posted by Bruce Thompson GQ on March 7, 2006 7:17 PM (e)

Is anyone ready to email the authors with their questions? Or would that take the fun out of the discussion?

Delta Pi Gamma (Scientia et Fermentum)

Comment #84804

Posted by 'Rev Dr' Lenny Flank on March 7, 2006 7:32 PM (e)

Hey Blast, why have Dr Fry and every other scientist you have ever talked with here, all unanimously stated that you’re full of crap?

Why do you suppose that is, Blast?

Comment #84810

Posted by Faidon on March 7, 2006 7:48 PM (e)

To any lurkers out there, the Darwinists are stymied by my arguments, and instead of rebutting the arguments, they spread venom. All of this so as to create the impression of: “How can all these people be wrong, and this other guy (who they call all kinds of names) be right.” That’s their way of “winning” arguments. Fascists would be proud.

Oh don’t worry, the lurkers are still here, Blast… we’re still waiting for you to answer to this:

Popper's Ghost wrote:

p. 157. “Colonies had variable morphologies, even during the steady-state phase, but the majority were roughly spherical, usually with eight (but occasionally four) cells per colony.” That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4). Anything else is a ‘multicell.’ And, yes, a “multicell” is a large—a very large (LOOK AT the PICTURE)—‘colony’, which, apparently, reproduces differently than the ‘true’ 8-celled ‘colonies’; i.e., they ‘bud’.

Why did Blast start his highlight just after the word “usually”? Does it possibly have anything to do with being, um, DISHONEST?

And also this:

Anton wrote:

I suspect it’s the same reason as why he quoted:

p.160 “The Chlorella had maintained the normal unicellular body shape for thousands of generations in the same laboratory culture conditions. After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

and failed to highlight the “After about 10-20 generations in the presence of the phototroph.”

Seems that your exit strategy (I’ll wait ’till they’re fed up refuting me and start not paying much attention, then I’ll razzle dazzle them with a long blabbering post and immediately declare “case closed” and depart claiming moral victory) didn’t quite work, eh?
Even we ignorant lurkers are familliar with ‘The Ways Of The Internets’, and recognize those who use them: And the insincerity in your posting is not that hard to detect. I was a fool not to notice it before, unfortunately.
But hey, since you value our opinion so much, please try and prove you have something to say more substantial than “oh oh, they didn’t show all data, that obviously means the data they hide must be totally disproving their theory somehow”.
I’ll just go grab a soda; this is getting interesting.

Comment #84816

Posted by 'Rev Dr' Lenny Flank on March 7, 2006 8:19 PM (e)

To any lurkers out there, the Darwinists are stymied by my arguments, and instead of rebutting the arguments, they spread venom.

Speaking of “venom”, Blast, let’s remind everyone what Dr Fry said to you the LAST time you shot your mouth off with a scientist in the room:

As I mentioned before, venom toxins are NOT modified salivary proteins. Rather they are the mutation of a normal body protein for the use as a toxin. There is not a magic little amino acid sequence added on but rather changes to existing functional residues or rearrangement of molecular scaffold. All of which is new information as this is occuring on a duplicate gene to the normal body protein, not to the body protein itself.

Venom evolution is much easier to understand if you follow the data trail rather than trying to shoe-horn it into a prepackaged theory that is particularly useless.

In other words, read the papers I’ve already referenced above.

Read those papers yet, Blast?

Or do you prefer to get your, uh, science information from “ecological visionaires”. (snicker) (giggle)

Comment #84837

Posted by BlastfromthePast on March 7, 2006 11:47 PM (e)

Faidon wrote:

Oh don’t worry, the lurkers are still here, Blast… we’re still waiting for you to answer to this: ….….(from earlier post) Why did Blast start his highlight just after the word “usually”? Does it possibly have anything to do with being, um, DISHONEST?

Are your really saying this has to be answered?!!? This is pathetic: Here’s the (obvious) answer: The ‘colonies’ are ‘usually’ 8-celled; but sometimes they’re 4-celled. See how hard that was to answer? So, now, tell me, Faidon, what was it exactly I was trying to conceal?

As to the “10-20 generations”, first, let’s notice that the author is not saying it took 10-20 generations for the 8-celled colony to “appear”, but to become dominant. Secondly, I addressed this very question in the very long post from two days ago. Please read it. And Faidon, I hope you can understand it. You don’t appear to follow arguments very well.

RDLenny Flank wrote:

Read those papers yet, Blast?

Indeed, I have Lenny. Rather thoroughly. And, now, for the fourth or fifth time, I’m telling you that the good Dr. Fry had no answer in those papers to my question about gene recruitment. The fact that you keep asking this stupid question only proves that YOU haven’t read the papers, or else you would have believed me the first time I gave you the answer.

You also have included a quote from the good Dr. Fry, part of which reads: “Venom evolution is much easier to understand if you follow the data trail rather than trying to shoe-horn it into a prepackaged theory that is particularly useless.”

But, of course, this is what Darwinists do every day of the week! His explanation of the ‘modified’ proteins that make up snake venom does NOT explain why these proteins are being ‘expressed’ in the saliva glands, now does it? Where did that ‘information’ come from? Does he have an explanation? It’s not just some ‘magical amino acid’ that is added onto some regulatory protein, you know.

PvM wrote:

Yes, why don’t you Blast. So far you have been not only shown to be wrong about irrefutable but your assertions that the authors somehow omitted critical data is both an insult to these authors as well as to common logic.

Well, Pim, I see that you really aren’t a gentleman. And I see you’re not very smart as well.

By what logic have I been shown to be ‘wrong’ about ‘irrefutable’? Does this question about what, exactly, showed up only 70% of the time ‘refute’ my logic? Is this what you think?

Well, pay attention,…….THERE IS NO LOGIC INVOLVED in determining whether or not the 70% applies to the 8-celled colonies or not. That is SIMPLY A FACT–one way or the other. What logic is involved in making an observation?

Now, I challenge you: refute the logic I use in rejecting RM+NS as a mechanism in explaining the results of this experiment. And, oh, Pim, I took into count the reduced concentration of the Chlorella. So, good luck.

And, BTW, did I really ‘insult’ the authors? Well, the kind of reaction you’re demonstrating amply illustrates that Darwinists are willing to sink to the deepest of depths to defend their orthodoxy. So your behavior only makes any suspicion I have more probable–if they’re anything like the bunch of you.

You’re really a pathetic, pathetic group.

I think you’ve finally convinced me that you’re a complete waste of my time. You don’t deserve to be challenged. You’re not worthy of it.

Comment #84840

Posted by Sir_Toejam on March 7, 2006 11:58 PM (e)

sicne there is really little point in addressing the inherent misunderstandings and lack of logic you so regularly promulgate, let’s figure out why exactly you are trying to make a martyr of yourself hre on PT.

let’s go back to your statement here:

I once had an opportunity to do research. And guess what? The PhD. I was working for wanted to fudge our results on a grant application.

is this the true source of your martyrdom?

didn’t you tell us that grad school was merely a stepping stone to med school?

sounds more like an excuse, to me.

care to elaborate?

Comment #84842

Posted by Sir_Toejam on March 8, 2006 12:05 AM (e)

THERE IS NO LOGIC INVOLVED

yes, shake your fist harder, boy.

maybe if you scream loud enough, the heavens will split, black will become white, and your repeated drivel will all of a sudden become the wisdom of the ages.

come on now, let’s face your demons together, shall we?

I have a working theory that you are using what happened to you as a grad student as an excuse for your poor performance professionally.

In fact, your failure is so profound that you have ben forced to construct an elaborate defense mechanism, that involves serious denial and projection.

You apparently want to use what happened to you in grad school as the starting point for the excuse your life has become, so that’s as good a place as any to start.

What was your immediate reaction when you discovered that your prof. wanted to “fudge” data in order to better obtain grant money?

It sounds like it had a serious impression on you.

How shocking was the revelation, really?

Comment #84844

Posted by PvM on March 8, 2006 12:30 AM (e)

PvM wrote:

Yes, why don’t you Blast. So far you have been not only shown to be wrong about irrefutable but your assertions that the authors somehow omitted critical data is both an insult to these authors as well as to common logic.

Well, Pim, I see that you really aren’t a gentleman. And I see you’re not very smart as well.

For pointing out how you are misbehaving. Tsk Tsk.

By what logic have I been shown to be ‘wrong’ about ‘irrefutable’? Does this question about what, exactly, showed up only 70% of the time ‘refute’ my logic? Is this what you think?

Nope it shows how your claim about irrefutable becomes quite shakey.

Well, pay attention,…….THERE IS NO LOGIC INVOLVED in determining whether or not the 70% applies to the 8-celled colonies or not. That is SIMPLY A FACT—one way or the other. What logic is involved in making an observation?

I am impressed that you are admitting that there is no logic involced here but the 70% applies to all cases. In 70% of the cases, however a dominant 8 multicell colony arose. Simple…

Now, I challenge you: refute the logic I use in rejecting RM+NS as a mechanism in explaining the results of this experiment. And, oh, Pim, I took into count the reduced concentration of the Chlorella. So, good luck.

You have ignored the stated reasons and you have made up 3 ‘arguments’ one of which has to be outright rejected, the other two ignore the dynamics of chemostats.

And, BTW, did I really ‘insult’ the authors? Well, the kind of reaction you’re demonstrating amply illustrates that Darwinists are willing to sink to the deepest of depths to defend their orthodoxy. So your behavior only makes any suspicion I have more probable—if they’re anything like the bunch of you.

So far it has been your own behavior which has been exemplifying how deep some want to sink.

You’re really a pathetic, pathetic group.

I think you’ve finally convinced me that you’re a complete waste of my time. You don’t deserve to be challenged. You’re not worthy of it.

When were we challenged? You have yet to come close to challenge this group with much of any argument of logic. In addition you have shown that your reading comprehension is a bit lacking. Of course, your attitude towards the authors further exemplifies the lack of depth to your arguments which seem to be mostly based on insinuation and some hand waving.

Feel free to leave. While I regret having lost such a ‘great defender of the faith’, there are more worthy causes.

Btw lets work down the list

Blast wrote:

1.) In EVERY replicate of this experiment, the 8-cell ‘colony’ is observed and becomes permanent.

2.) The presence of 100+-cell ‘colonies’ cannot be explained via the ‘mutation’ of the Chlorella ‘unicells’ either through ‘induction’ by the presence of a predator, or through these ‘mutations’ being present in the culture before the experiment began.

3.) Photographic evidence strongly suggests that clusters larger than the 8-cell ‘colonies’ are the product of a clustering of 8-cell ‘colonies’. The persistent presence of 24-cell ‘colonies’, which defies the geometric progression of cell division, buttresses this observation.

1 has been shown to be based on a reading comprehension problem, 2 is based on the flawed concept that a mutation arose. In fact more likely is that the genetic variant was present in the original sample at much lower concentrations lets say 0.0001. However when the chlorella were being eaten these ‘few’ survived and continued to be more succesful in reproduction than their unicellular counterparts. Within 5 days most of the chlorella had ended up being eaten when the colony recovered, this time with a significant part being multicellular colonies cell count >100. Check out some of the published work on chemostat dynamics with prey/predators. Your handwaving arguments, while superficially plausible fail.

Blast wrote:

nd according to geometric growth, that’s 2^7 times growth starting with one dividing ‘mutant’ cell; in other words, 7 generations worth of growth.

Flawed premise, flawed conclusion. You are still assuming that a single mutation arose. Check out the papers on genetic variation of chlorella or other such colonies where rare variants are present in much lower concentrations. Why is it that people have such a simplistic view of evolution where any genetic variation is fully lacking? sigh…

As far as number 3, the 24 cell colonies are concerned, a more careful reading of the paper would have resolved this question. In fact colonies were observed with few of its cells dividing, in other words the factor 2 argument is more of a strawman.

Look Blast, I applaud your effort but you really lost it when you started to accuse the authors of nefarious motives… That would have been a good time to remain silent and admit that had been mistaken. Instead you chose a path which has caused you nothing but pain as it exposed a side of you few had seen before.

Why is it so hard for you to accept that the data strongly support a Darwinian scenario? Especially when I point out that a Darwinian scenario does not match your scenario in which a single mutation arises and spreads rather than the more likely scenario of a population with a small fraction of genetic multicellular variants which get amplified under predation and selection?

Comment #84846

Posted by Sir_Toejam on March 8, 2006 12:54 AM (e)

it exposed a side of you few had seen before

hmm, methinks perhaps you haven’t been paying attention to the history of Blast’s posting behavior.

check the thread on the evolution of snake venoms that lenny and I referred to.

same logic, same behavior; and that’s certainly not the first time.

Why is it so hard for you to accept that the data strongly support a Darwinian scenario?

I’m working on trying to find that out - see the post above yours.

I’m going on the theory that he is commiting voluntary martyrdom through extensive projection and denial.

the one thing he HASN’T done before is start mentioning his experience as a grad student (brief as it was).

I think there is where at least one of his demons lie, and since he earlier stated his willingness to explore that area, it sure sounds more interesting and productive than continuing the always pointless attempt to address the logical flaws in his reasoning and analytical skills.

Comment #84855

Posted by BlastfromthePast on March 8, 2006 1:58 AM (e)

PvM wrote:

2 is based on the flawed concept that a mutation arose. In fact more likely is that the genetic variant was present in the original sample at much lower concentrations lets say 0.0001.

First, if you read my post, I said that if it assumed ‘as Pim did’ that the mutation was there from the beginning, then the concentrations were TOO HIGH. I calculated a concentration of roughly 0.004 times the original density. The orginal density was 2.0 x 10^6 cells/ml. That results in the presence of the ‘100+-cell mutant’ of 8 x 10^3 cells/ml. This almost 10,000 100+-cell ‘colonies’ per ml. This is very high. The very point I was making there was that it was TOO HIGH. It would have been seen. How do you miss such a concentration in the ‘original culture’?

So now, allow me to quote from the article: “In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continous cultures.” (p.154) And, “During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a)” (pp.156-157) Using microscopic screens, you couldn’t have missed a mutant population that large BEFORE the experiment. The logical conclusion is that it WASN’T there.

Second, there is also the problem of the absence of 16-celled ‘colonies’ and the presence of 24-celled ‘colonies’. If the geometric progression is 2,4,8,16,32,…..up to the 100+-cell colonies, then where are the 16-celled forms, and how do you explain the 24-cell ‘colonies’ (see Fig 2b)?

PvM wrote:

As far as number 3, the 24 cell colonies are concerned, a more careful reading of the paper would have resolved this question. In fact colonies were observed with few of its cells dividing, in other words the factor 2 argument is more of a strawman.

What do you propose, then, is the mechanism of growth? And, if not all the cells were dividing, then it should have taken the Chlorella 100+-cell ‘colonies’ even longer to duplicate, which now makes the original concentration even higher, and, thus, even more evident ‘before’ the experiment. What say you?

And you once again appear to be a gentleman. Now let’s see how smart you are! ;)

As to the author’s intentionally witholding information, you’re right, that’s not the kind of thing to insinuate without more proof. But it sure behooves me why they thought it unimportant to publish. If you have the data, then why not publish it?

Comment #84860

Posted by PvM on March 8, 2006 2:29 AM (e)

First, if you read my post, I said that if it assumed ‘as Pim did’ that the mutation was there from the beginning, then the concentrations were TOO HIGH. I calculated a concentration of roughly 0.004 times the original density. The orginal density was 2.0 x 10^6 cells/ml. That results in the presence of the ‘100+-cell mutant’ of 8 x 10^3 cells/ml. This almost 10,000 100+-cell ‘colonies’ per ml. This is very high. The very point I was making there was that it was TOO HIGH. It would have been seen. How do you miss such a concentration in the ‘original culture’?

Do you really realize what you are saying here? The relative frequency is 0.004, that’s quite a small number to actually detect. 4 in every thousand algae would be multicellular.

So now, allow me to quote from the article: “In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continous cultures.” (p.154) And, “During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a)” (pp.156-157) Using microscopic screens, you couldn’t have missed a mutant population that large BEFORE the experiment. The logical conclusion is that it WASN’T there.

Wrong again.

I am a student of M. E. Boraas, so I’m familiar with the techniques used in this work. This particular alga is about 2 - 4 um in diameter. When we grow them in a chemostat (without the predator) we get a density on the order of 3 X 10 ^ 7 cells per ml! If a pre-existing variant is present at a frequency of 0.0001 we would, on average, see it only once in 10,000 counted. To be sure of catching it at this frequency, we would have to count an incedible amount of cells! (Just as a point of information, when we do direct counts, we usually count 300-500 cells in a sample. This is in accord with phycological and bacteriolgical practice).

Second, there is also the problem of the absence of 16-celled ‘colonies’ and the presence of 24-celled ‘colonies’. If the geometric progression is 2,4,8,16,32,…..up to the 100+-cell colonies, then where are the 16-celled forms, and how do you explain the 24-cell ‘colonies’ (see Fig 2b)?

As far as number 3, the 24 cell colonies are concerned, a more careful reading of the paper would have resolved this question. In fact colonies were observed with few of its cells dividing, in other words the factor 2 argument is more of a strawman.

What do you propose, then, is the mechanism of growth? And, if not all the cells were dividing, then it should have taken the Chlorella 100+-cell ‘colonies’ even longer to duplicate, which now makes the original concentration even higher, and, thus, even more evident ‘before’ the experiment. What say you?

And you once again appear to be a gentleman. Now let’s see how smart you are! ;)

Why are you wearing sneakers said one hiker to his hiker friend? … In case we meet up with a mountain lion. But you cannot outrun a mountain lion… But I do not need to, all I need to do is outrun you…
As I explained partial cell division, tearing off are all relevant observations

As to the author’s intentionally witholding information, you’re right, that’s not the kind of thing to insinuate without more proof. But it sure behooves me why they thought it unimportant to publish. If you have the data, then why not publish it?

Seems you have not really published much of anything or you would know the answer. And it’s trivial.

Comment #84861

Posted by Sir_Toejam on March 8, 2006 2:41 AM (e)

you just can’t resist, can you blast?

I thought you were done with us “lowly darwinists” who weren’t worthy of the proclamations of Zarathustra?

since you said you had no problems exploring your all too brief graduate career, why don’t you want to talk about it now?

Comment #84862

Posted by PvM on March 8, 2006 2:47 AM (e)

And why focus on 24? What about 20 for instance or any other number not a multiple of 2?

Irrefutable evidence ? Or just a bit of grandstanding. Let me give you a hint, there are some good models for prey-predator interactions in a chemostat. Perhaps you should give it a try and see of the numbers do not add up?
I have seen several simulations and actual data which mimick the data observed here quite nicely.

So lets consider some of these ideas you mention that the initial concentration dropped to 0.1% or 0.001 the original value.
You also mentioned 0.004 for the original concentration of the multicellular. This means that the relative concentration went from 0.004 to 4
Somehow these irrefutable numbers do not seem to add up to support your thesis.

Comment #84864

Posted by Sir_Toejam on March 8, 2006 3:25 AM (e)

I think you’ve finally convinced me that you’re a complete waste of my time

I can’t get over this.

he finally says something absolutely correct, and then comes right back anyway.

face it, blast you WANT us to deride you.

you WANT to be a martyr.

you’re not doing a very good job of it tho.

Comment #84956

Posted by Faidon on March 8, 2006 2:40 PM (e)

Whatever, Blast. You don’t appear to make arguments very well:

first, let’s notice that the author is not saying it took 10-20 generations for the 8-celled colony to “appear”, but to become dominant. Secondly, I addressed this very question in the very long post from two days ago.

Well, yes you did, and thank you for now replying to your own subsequent question:

Thus, when they say that ‘multicells’ appeared in 70% of the replicates, [‘multicellular forms’, not ‘multicells’ -I pulled a little DaveScott here :)] and then say that an 8-cell colony became the dominant phototroph in ALL replicates, why is it you infer that the 8-celled colonies only appeared in 70% of the replicates? How does this follow?

You see, what you are desperately trying to conceal is how bogus your

“Because I say so, multicellularity only refers to ‘multicells’ alone, which are not colonies, just large multicellular colonies only they’re not colonies because colonies are strictly defined as 8-cell structures only they’re not actually you know whatever CASE CLOSED”

argument is.

You should have dropped it from the beginning claiming their “vague description” got you confused; by now noone would remember it and you’d have maintained some shreds of credibility.

But it seems the #1 rule in your Handbook For the Internet Debater says: “Never, ever fall back on an argument you made, not for the most trivial sideissue whatsoever”.

So, you got carried away and tried to back it up using absurd self-assumed “definitions” and obvious selective quoting, and now everyone knows you for what you are.

Better luck next time.

Comment #85139

Posted by BlastfromthePast on March 9, 2006 6:59 AM (e)

PvM wrote:

BlastfromthePast wrote:

So now, allow me to quote from the article: “In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continous cultures.” (p.154) And, “During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a)” (pp.156-157) Using microscopic screens, you couldn’t have missed a mutant population that large BEFORE the experiment. The logical conclusion is that it WASN’T there.

Do you really realize what you are saying here? The relative frequency is 0.004, that’s quite a small number to actually detect. 4 in every thousand algae would be multicellular.

Yes, I do. And this 0.004 was calculated using a very conservative approach. We’ll continue with the next quote, which I just have to assume is something you wrote, Pim, although it’s in a quote box:

PvM ?? wrote:

Wrong again….If a pre-existing variant is present at a frequency of 0.0001 we would, on average, see it only once in 10,000 counted. To be sure of catching it at this frequency, we would have to count an incedible amount of cells! (Just as a point of information, when we do direct counts, we usually count 300-500 cells in a sample. This is in accord with phycological and bacteriolgical practice).

(My emphasis)

Not an incredible amount really. If the cells are spread out randomly–which is safe to assume–then every time you count a cell, you have a chance to ‘see’ one of the ‘multicells’. Which means that in each sample taken, you have a (300-500) x .004 chance of ‘seeing’ the ‘multicell’. That means you have a 12-20% chance of seeing the multicell in each sample. Thus, in every 5 samples taken (this is a two decade old culture), you should run across 1 multicell. And, so, I repeat, “you couldn’t have missed a mutant population that large BEFORE the experiment.”

PvM wrote:

BlastftPast wrote:

PvM wrote:

BlastftPast wrote:

Second, there is also the problem of the absence of 16-celled ‘colonies’ and the presence of 24-celled ‘colonies’. If the geometric progression is 2,4,8,16,32,…..up to the 100+-cell colonies, then where are the 16-celled forms, and how do you explain the 24-cell ‘colonies’ (see Fig 2b)?

As far as number 3, the 24 cell colonies are concerned, a more careful reading of the paper would have resolved this question. In fact colonies were observed with few of its cells dividing, in other words the factor 2 argument is more of a strawman.

What do you propose, then, is the mechanism of growth? And, if not all the cells were dividing, then it should have taken the Chlorella 100+-cell ‘colonies’ even longer to duplicate, which now makes the original concentration even higher, and, thus, even more evident ‘before’ the experiment. What say you?

As I explained partial cell division, tearing off are all relevant observations

Doesn’t the article actually suggest a unsynchronized dividing of cells? Which only means that at any one time you may have an ‘odd’ number of cells. But why isn’t there any 16-cell, or 17, or 18, or 19 that show up? In the next post, you mention 20 cells. But 20 cells is likely two 8-celled and one 4-cell colony stuck together. I don’t see how that explains the data of Fig. 2.

Additionally, this sounds like an overall ‘slower’ division process, which then makes it more improbable that a mutation appeared, and more ‘probable’ that the mutant would be seen before the experiment (the relative frequency number would calculate out higher). So my analysis of the data stand, and the only logicl conclusion is that what we’re seeing is chemical induction of the Chlorella, since RM+NS is ruled out.

PvM wrote:

BlastftPast wrote:

And you once again appear to be a gentleman. Now let’s see how smart you are! ;)

Why are you wearing sneakers said one hiker to his hiker friend? … In case we meet up with a mountain lion. But you cannot outrun a mountain lion… But I do not need to, all I need to do is outrun you…

I like your sense of humor. You’ve got panache.

PvM wrote:

BlastftPast wrote:

But it sure behooves me why they thought it unimportant to publish. If you have the data, then why not publish it?

Seems you have not really published much of anything or you would know the answer. And it’s trivial.

But that’s the trivial answer. Sure it might be trivial. But on the other hand, if you want to disprove the chemical induction ‘hypothesis’, then the two critical parts of that demonstration are the onset of morphological change and the regress to the original morphology. That makes it pertinent. They do us a great disservice by not publishing it no matter how poor, or seemingly insignificant, it may seem.

Comment #85154

Posted by BlastfromthePast on March 9, 2006 7:27 AM (e)

Faidon wrote:

You see, what you are desperately trying to conceal is how bogus your

“Because I say so, multicellularity only refers to ‘multicells’ alone, which are not colonies, just large multicellular colonies only they’re not colonies because colonies are strictly defined as 8-cell structures only they’re not actually you know whatever CASE CLOSED”

argument is.

The ‘70% of replicates’ remark occurs on page 157.

On page 157, the words colony/colonies appears 20 times; the word multicells 1 time. So why would you want to think that what they say about ‘multicells’ somehow applies to ‘colonies’ even though the word isn’t found in the very sentence you say applies to the ‘colonies’?

When there is a sentence that uses both the words ‘colonies’ and ‘replicates’, it reads: “After about 10-20 generations in the presence of the phagotroph, an eight-celed Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

They distinguish between ‘multicell’ and ‘colony’. They mention one, then the other, in sentences that contain the word replicates. When the mention ‘multicell’, they say it ‘appears’ in 70% of the replicates. When they mention ‘colony’, they say the 8-celled ‘colony’ became dominant in ALL replicates. If it became the dominant phototroph in ALL replicates, then obviously it was present in ALL replicates.

That’s my logic. What’s yours?

Comment #85235

Posted by PvM on March 9, 2006 10:52 AM (e)

A more charitable reading of the paper suggests that in 70% of the experiments multicells arose, in all of those (70%) cases this included an 8 cell variant which became dominant in all cases.

Comment #85240

Posted by PvM on March 9, 2006 11:08 AM (e)

the quote about 0.0001 was not mine but Boxhorn, one of the co-authors of the paper, in a response to an ASA discussion. 1 in 10,000 would be a variant and thus when looking at 500 cells you have a pretty small chance to see a multicell form.

You make much of the statement

Flagellates and Chlorella unicells in this steady state had population densities reduced to about 0.1% of their maximum numbers during the transient phases.

But this is the steady state solution. We are looking for the transient effects. Take the 0.1% and 0.0001 fraction of multicells would now become 0.1. Once an insiginificant fraction these multicells now become a significant fraction. After 12 days the the biovolume of the multicells is 37 times that of the unicells. After 40 days the fraction of 8 cells is about 10 times that of unicells which are at 0.1% of their original level suggesting that the multicells have reached a level of 1% of the original. The reason why > 100 increases in relative size is because the unicells decrease in numbers… (figure 2b)

Comment #85244

Posted by Anton Mates on March 9, 2006 11:21 AM (e)

BlastfromthePast wrote:

The 70% of replicates’ remark occurs on page 157.

On page 157, the words colony/colonies appears 20 times; the word multicells 1 time. So why would you want to think that what they say about ‘multicells’ somehow applies to ‘colonies’ even though the word isn’t found in the very sentence you say applies to the ‘colonies’?

Oh, for God’s sake. The whole point of synonyms is that you get to alternate their use. Why in the world would you use them in the same sentence?

Look:

Two potential mechanisms for reducing colony size were suggested from electron micrographs of multicellular Chlorella. First, the original mother cell wall became increasingly fragile in multicells. The enclosing membrane of colonies from cultures 20±100 days old had a ‘ropy’ appearance (Fig. 1a).

Hence, the unicellular Chlorella are within the preferred size range and mature Chlorella colonies are just outside the range ingested by O. vallescia. We did not detect any obvious shift in size of prey captured by these Ochromonas. It is likely that we would have not been able to detect shifts in prey morphology without a relentless, unshifting predation pressure on a particular prey size. Counter-shifts in the predator might well have eliminated the multicells before they could proliferate.

© A large, multicellular Chlorella colony subjected to 8 days of grazing by Ochromonas.

In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the light, the multicellular form was slowly displaced by unicells (data not shown).

“Colony” = “multicellular form” = “multicell.” This is how the paper uses the terms, and this is what basic knowledge of the English language would indicate unless the authors specifically distinguish them from one another. Are you trying to make your claim to have taken biology courses seem more credible by demonstrating that you weren’t taking English classes instead?

Comment #85377

Posted by BlastfromthePast on March 9, 2006 4:02 PM (e)

“Colony” = “multicellular form” = “multicell.” This is how the paper uses the terms, and this is what basic knowledge of the English language would indicate unless the authors specifically distinguish them from one another. Are you trying to make your claim to have taken biology courses seem more credible by demonstrating that you weren’t taking English classes instead?

Not to infuriate you, Anton, but isn’t this just another ad hominem argument?

From the legend for Fig. 1a. “The colony apparently is breaking apart due to growth of component eight-celled colonies.

From Fig. 1c.: “A large, multicellular Chlorella colony……all cells in the colony appear to adhere by membranes.

English 101: ‘Multicells’ “adhere by membranes. ‘Colonies’ are made up of “component eight-celled colonies”….which adhere to one another–just as my chemical induction hypothesis suggests they would. That’s why you see 24-celled ‘colonies.’

And, of course, “8-celled colonies became the dominant phototroph in ALL replicates.”

Comment #85404

Posted by BlastfromthePast on March 9, 2006 4:46 PM (e)

PvM wrote:

the quote about 0.0001 was not mine but Boxhorn, one of the co-authors of the paper, in a response to an ASA discussion. 1 in 10,000 would be a variant and thus when looking at 500 cells you have a pretty small chance to see a multicell form.

First, is there someplace online that we can access this discussion?

Second, it appears that someone was questioning their reasoning along basically the same lines that I have.

Third, yes, 0.0001 is small. But, again, statistically if every time you ‘count’, you count 300 to 500 cells, that means each time you have a 3 to 5% chance of ‘seeing’ this variant. (Can a ‘colony’ of eight cells not catch your eye in a sea of ‘unicells’?) They kept this ‘unicell’ culture going for 20 years. It’s hard to believe that they never encountered this ‘variant’ in all these years.

Fourth, it’s entirely possible that they didn’t ‘see’ ‘multicellularity’ until they saw the 100+-celled Chlorella. If, during the years, there were, indeed, 8-celled ‘colonies’ present in the cell counts, these might have looked to them like no more than ‘mother cells’. This putative failure on their part is entirely consistent with my hypothesis that induction of the ‘mother cell membrane’ is what we, in fact, see taking place in the experiment. Again, how important the data is for what they term the ‘slowly dissolving’ ‘colonial forms’. The key aspect: empty mother cell membranes.

Comment #85543

Posted by Anton Mates on March 9, 2006 11:01 PM (e)

BlastfromthePast wrote:

“Colony” = “multicellular form” = “multicell.” This is how the paper uses the terms, and this is what basic knowledge of the English language would indicate unless the authors specifically distinguish them from one another. Are you trying to make your claim to have taken biology courses seem more credible by demonstrating that you weren’t taking English classes instead?

Not to infuriate you, Anton, but isn’t this just another ad hominem argument?

No fury necessary–the last sentence certainly is one. As I mentioned before, ad hominem arguments are appropriate when evidence is provided by a non-credible source. (I wasn’t really being serious here, though. I don’t believe you’re honestly that bad at reading comprehension; you know as well as the rest of us that this “colonies and ‘colonies’ and multicells are different” claim is untenable.)

From the legend for Fig. 1a. “The colony apparently is breaking apart due to growth of component eight-celled colonies.”

You fail to mention that this is from a culture 240 days after predator inoculation–well after the eight-celled colonies have come to dominate the culture. IOW, this is an eight-celled colony, just an end-stage one that’s fissioning. Ironic–even as you argue that “multicells” and “colonies” are different things, you confuse them yourself!

From Fig. 1c.: “A large, multicellular Chlorella colony……all cells in the colony appear to adhere by membranes.

Which, since that colony has dozens of cells, directly refutes your claim that “That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4).”

‘Colonies’ are made up of “component eight-celled colonies”….which adhere to one another—just as my chemical induction hypothesis suggests they would. That’s why you see 24-celled ‘colonies.’

Ah, so this paper is actually a work of poetry, and “colony” is secretly intended to have two completely different meanings! Thank God you’re here to work out Boraas’ complex system of metaphor for us.

So why is it that, according to figure 2a), we also see colonies–or ‘colonies,’ take your pick–of size 2, 5, 7, 9, 18-19, 75 and so forth?

And, of course, “8-celled colonies became the dominant phototroph in ALL replicates.”

Remarkable. You started off by quoting:

“After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

and simply failing to highlight the first part of the sentence. Now that this has been repeatedly pointed out, you’re actually substituting your own paraphrase which doesn’t even have the first part. You’ve outdone yourself.

Comment #85555

Posted by BlastfromthePast on March 9, 2006 11:30 PM (e)

This Boxhorn fellow is very interesting, Pim.

I’ve been looking around. Seems like he’s very popular at Talk.Origins.com. Does this impeach his objectivity any?

Leaving that aside, I did learn some things.

One thing I learned is that the ‘growth rate’ on continuous culture is equal to the dilution rate. And the dilution rate is =inflow rate/bottle vol. I learned normal chemostat bottles do, indeed, have a 500ml experimental fluid capacity.

So I looked back at the paper. It seems that they report the inflow rate as 0.035 ml/hr. Well, that’s just wrong. This number gives you an unbelievably small growth rate. The number should be 0.035 liter/hr, meaning 35 ml/hr. When you do the calculation, you come up with a growth rate of 1.68 days. We’ll call it 1.7 days. This is roughly what I calculated using numbers off of Fig 2a. and 2b. But I thought that too high, based on what the authors had written. But, lo and behold, according to Boxhorn’s own calculation, the growth rate (doubling time) is 1.7 days.

If you look at the article, you’ll see that the chlorella is grazed down, peaks again, and is re-grazed back down—all in 12 days. As I (conservatively) argued before, we cannot expect any chemical signal to be sent for at least 3 days after inoculation of the predator. According to the paper, after 10 days (p.156-7) “the prey Chlorella now included colonial forms as well as ‘unicells’ (10 days, Fig 2a). The number of cells per colony ranged from four to hundreds (Fig. 1c)……..During a second cycle of flagellate growth and Chlorella decline (16 days, Fig. 2a), the Chlorella colonies persisted while the Chlorella ‘unicells’ declined to 1% of the total cells in the culture.”

So, the first sign of ‘colonies’ is reported as being Day 10. By Day 16 the ‘unicells’ were down to 1%. Now 10 days (sighting of ‘colonies’) - 3 days (when signal kicks in) = 7 days. 7 days/1.7 days/generation = 4.2 generations.

[N.B., I suspect that it takes a combination of a very low ‘unicell’ “signal”, and a very high predator “signal” (which is likely a digestive by-product). Which means that the “signal” for the ‘colonies’ to form probably didn’t happen until Day 5. Then the number of days is: 10 - 5 = 5 days, with a resulting generations number of almost exactly 3. And, of course, to go from 1 cell to 8 cells requires….……drumroll, please…… 3 generations. How interesting, eh?]

Now, here, once again, is the authors’ FIRST reason for ‘discounting’ the chemical induction idea:

Colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates.”

Do you see something wrong here?

Was this an honest error?

Comment #85562

Posted by BlastfromthePast on March 9, 2006 11:55 PM (e)

Anton Mates, referring to Fig 1c, wrote:

Which, since that colony has dozens of cells, directly refutes your claim that “That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4).”

Here’s what the authors write on p. 159:

“In continous cultures with the predator, the rapid appearance of very large multicellularChlorella (Fig 1c) apparently resulted from incomplete division: an initial loss of the mechanism for separating successive generations.” (Note, this is exactly what I propose happens due to chemical induction.)

Anton, do you see the word ‘colony’ anywhere in this sentence? These “very large multicellular Chlorella” appear in 70% of the replicates, but the 8-celled ‘colonies’ appear in all replicates of the experiment.

Isn’t this straightforward by now?

Comment #85598

Posted by Anton Mates on March 10, 2006 1:26 AM (e)

BlastfromthePast wrote:

One thing I learned is that the ‘growth rate’ on continuous culture is equal to the dilution rate. And the dilution rate is =inflow rate/bottle vol. I learned normal chemostat bottles do, indeed, have a 500ml experimental fluid capacity.

So I looked back at the paper. It seems that they report the inflow rate as 0.035 ml/hr. Well, that’s just wrong. This number gives you an unbelievably small growth rate. The number should be 0.035 liter/hr, meaning 35 ml/hr.

I think you’re right that that’s an error–from looking over a few other papers it sems like typical dilution rates are orders of magnitude larger. However, it’s worth noting that no growth rate would be “unbelievably small” in a chemostat. Simply slow down the dilution rate and you can get the average growth rate as close to 0 as you want.

When you do the calculation, you come up with a growth rate of 1.68 days. We’ll call it 1.7 days.

That’s not what I get (and growth rate is measured per day, not in days). (.035 liter/hr) /(.5 liters) = growth rate of .07 per hr. Doubling time is ln(2)/growth rate = 9.9 hours.

That’s roughly two generations per day, which is consistent with Fig. 2 –the time between appearance and dominance of colonies was 6 days, which agrees well with the claim that that time is generally “10-20 generations.”

Of course this is only at steady state–we expect the growth rate to be temporarily higher after each dieoff. But not too much higher, I think; it doesn’t look (from a random Googletrawling so don’t take this as gospel) like Chlorella ever grows much faster than two generations per day.

This is roughly what I calculated using numbers off of Fig 2a. and 2b. But I thought that too high, based on what the authors had written. But, lo and behold, according to Boxhorn’s own calculation, the growth rate (doubling time) is 1.7 days.

Where are you getting that? I haven’t seen Boxhorn give a growth rate estimation for Chlorella.

So, the first sign of ‘colonies’ is reported as being Day 10.

[snipped]

Now, here, once again, is the authors’ FIRST reason for ‘discounting’ the chemical induction idea:

“Colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates.”

Do you see something wrong here?

Was this an honest error?

In your math, perhaps. By my calculations, 10 days is about 20 generations.

Comment #85603

Posted by Anton Mates on March 10, 2006 1:40 AM (e)

BlastfromthePast wrote:

Anton Mates, referring to Fig 1c, wrote:

Which, since that colony has dozens of cells, directly refutes your claim that “That’s their definition for a ‘colony’: A colony consists of 8 cells (sometimes 4).”

Here’s what the authors write on p. 159:

“In continous cultures with the predator, the rapid appearance of very large multicellularChlorella (Fig 1c) apparently resulted from incomplete division: an initial loss of the mechanism for separating successive generations.” (Note, this is exactly what I propose happens due to chemical induction.)

Anton, do you see the word ‘colony’ anywhere in this sentence?

Nope. Of course since “very large multicellular Chlorella” are colonies, and as amply demonstrated above that’s precisely how Boraas uses the latter term, it would be kind of silly to use both terms in one sentence, wouldn’t it?

Oh, but let’s look at the very next sentences, shall we?

“The most probable initial mechanism for colony formation, adhesion of the daughter cells to the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies (Fig. 1d) and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation). Incomplete cell division has also been proposed as a mechanism for selection of elongated bacteria in the presence of protozoan predation (Shikano et al., 1990; Gillott et al., 1993).”

Why, it turns out to be yet another paragraph where “multicellular Chlorella” and “colonies” are used interchangeably.

These “very large multicellular Chlorella” appear in 70% of the replicates, but the 8-celled ‘colonies’ appear in all replicates of the experiment.

Isn’t this straightforward by now?

Yep. You make that claim, I point out that the actual quote for the latter is

“After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella ‘colony’ became the dominant phototroph in all replicates of this experiment.”

which obviously does not imply that the eight-celled colony appears in all replicates. Then I realize that you’ll probably still claim that it does at least ten more times, despair, and shoot myself.

Comment #85661

Posted by W. Kevin Vicklund on March 10, 2006 3:50 AM (e)

Actually, Anton, it appears that from Boxhorn’s paper on Talk.Origins, the generation time of a steady-state chemostat is simply the inverse of the growth rate (he was referring to E. coli in the example, but it is apparent that it would apply here as well). So the equation per Boxhorn, correcting for the alleged error, is .035 l/hr / .5 l = .07 per hour. The generation time is therefore 1/.07=14.3 hours. That puts it at just over half a day, which agrees with what I’ve seen for the max rate. And 20 generations at 14.3 hours/generation = 286 hours, or 11.9 days. Exactly what we expect…

It looks like blast multiplied by 24 to change hours to days (.07*24=1.68).

Even if the flow-rate is as reported, it is not necessarily unfeasible. All it means is that under steady-state conditions, it takes about 600 days for a generation. Throw a predator in there, and the growth rate can jump to max (by all accounts around that magical .07 per hour number) if the concentration of prey falls low enough. While the predator is present, the generation time will actually be higher than inverse of inflow due to predation. The only real fly in the oinment is the predator-less mixed chemostat - we don’t really know how fast the replacement occured (though I guess it’s possible they stepped up the flow a bit to speed up the process there). But the point is, the growth rate formula Boxhorn gave is only valid for a steady-state predator-less chemostat.

Where the hell did blast get “slowly dissolving” from, anyway? It’s not in the article. Anyway, I’m not sure what he thinks the missing data will show wrt empty mother cell membranes. The evolutionary theory would have little to no empty membranes at the start of the predator-less mixed chemostat. The concentration of empty membranes would then steadily rise as the colonies got washed out and the culture was dominated by unicells. Does he think that the induction scenario would predict something different?

Btw, blast, not only did the authors encounter the variant throughout the 20 years, they did so at a rate (2 or 3 times a year) that would be predicted if they took weekly samples.

As far as colony v. multicell, the paper is nonsensical when taken as a whole if they have distinct meanings. Especially when compared to the abstract of the original paper. Sorry, but you are grasping at straws.

Comment #85718

Posted by Anton Mates on March 10, 2006 8:17 AM (e)

W. Kevin Vicklund wrote:

Actually, Anton, it appears that from Boxhorn’s paper on Talk.Origins, the generation time of a steady-state chemostat is simply the inverse of the growth rate (he was referring to E. coli in the example, but it is apparent that it would apply here as well). So the equation per Boxhorn, correcting for the alleged error, is .035 l/hr / .5 l = .07 per hour. The generation time is therefore 1/.07=14.3 hours. That puts it at just over half a day, which agrees with what I’ve seen for the max rate.

And 20 generations at 14.3 hours/generation = 286 hours, or 11.9 days. Exactly what we expect…

However, the generation time (which so far as I can tell is synonymous with doubling time) is not simply the reciprocal of the growth rate k. You have to multiply by ln(2), hence my figure of 9.9 hours. 1/k by itself gives you the time it takes for the population (ignoring deaths/washouts) to increase by a factor of e, not for it to double.

Mind you, I’m just assuming “generation time is defined as doubling time” by looking at a bunch of tutorials on population growth (some of them explicitly about chemostats) via Google. So far they’ve all agreed, but if you actually took a class on the subject and heard something different, please let me know. (I agree that Boxhorn may have defined it as you did in his “Mutation Studies” talk.origins contribution.)

It looks like blast multiplied by 24 to change hours to days (.07*24=1.68).

Ah, that makes sense.

Even if the flow-rate is as reported, it is not necessarily unfeasible. All it means is that under steady-state conditions, it takes about 600 days for a generation.

It’s just that that would be so far below Chlorella’s potential exponential growth rate that it would be kind of pointless to even use a chemostat. You’d be better able to sustain exponential growth with two buckets and an eyedropper! As you say, once the predator becomes fairly common the growth rate will spike, so it’s not a problem for the paper either way–it just seems very unlikely to me that their original culture would have been set up like that. But since all I know on this subject is from the magical Inter-Net….

Maybe Tara Smith could advise us? This probably falls within her area of expertise.

Comment #85731

Posted by W. Kevin Vicklund on March 10, 2006 9:10 AM (e)

Sorry, Anton, I didn’t mean to sound as if I was disputing the ln(2), I was just stating what Boxhorn implied, and then offering up the results based upon his method, since that is what blast should have calculated. It also gives a longer doubling rate and is therefore more charitable to his argument - yet still whips it like a rented mule.

ln(2)/k makes a lot of sense, because most will not be at time 0 of the reproduction cycle.

Comment #85738

Posted by k.e. on March 10, 2006 9:43 AM (e)

They could always take the “free” legal services of the “Thomas Moore law Center” (giggle) I’m sure those guys will do a *splendid* job.

But they have to take Larry’s advice DON’T SAY the G-word….ah that leaves them nothing else to say except we don’t know how evolution happened and we don’t *like* it….muffle mumble, ace spaliens, tarot cards, astrology, er you know who, wink wink, nudge nudge

In which case if I was on the opposing team I would take the Dr. Miller approach and point out that the stickers don’t go far enough and complete the loop by saying evolution is THE ONLY theory that explains ….er how life evolved.


Dem Bones Dem bones Dem Dry Bones
Jaw bone connected to the ear bone Oh hear de word o’ de lord.
Dem bones, dem bones gonna vibrate
Oh hear the word o’ de Lord

Comment #85739

Posted by k.e. on March 10, 2006 9:44 AM (e)

opps wrong thread …sorry

Comment #85752

Posted by Anton Mates on March 10, 2006 11:08 AM (e)

W. Kevin Vicklund wrote:

Sorry, Anton, I didn’t mean to sound as if I was disputing the ln(2), I was just stating what Boxhorn implied, and then offering up the results based upon his method, since that is what blast should have calculated.

I think your reading of Boxhorn is quite correct; he apparently chose to define “generation time” as “average lifespan of an organism within the culture.” I dunno if that’s a common definition or not–haven’t seen it anywhere else–but in this case it was probably inappropriate. He’s calculating the number of mutations per unit time in a population, so the relevant quantity is the time necessary for a population’s worth of new cells to appear, which is of course the doubling time.

(Now let’s see if a microbiologist pops up to tell us we don’t know what we’re talking about….)

It also gives a longer doubling rate and is therefore more charitable to his argument - yet still whips it like a rented mule.

Right…both ways of calculating it give results close on either side of “two generations a day,” which as you say is just what the paper indicates.

Comment #85818

Posted by Anton Mates on March 10, 2006 4:40 PM (e)

Sir_Toejam wrote:

is this the true source of your martyrdom?

didn’t you tell us that grad school was merely a stepping stone to med school?

I still don’t believe Blast was ever actually a graduate student in a biological discipline. I mean, he considers exponential growth remarkable, he calls Chlorella “zooplankton,” he doesn’t think “evolution” includes changes in allele frequencies over time, he thinks there’s a universal uniform mutation rate in all organisms, he doesn’t believe that a culture can only provide light & nutrients at a finite rate, he thinks most mutations are harmful, he confuses “genome” with “chromosome”, he thinks an organism can only wash out within a chemostat if it “isn’t growing and multiplying”, he thinks a given phenotypic change can only be produced by one mutation within the entire genome…

And, to pick up where I left off a while ago, he’s still saying very very strange things for anyone who’s ever taken undergrad intro bio courses.

From this post alone:

Blast continues to misunderstand the concept of fitness:

All of the above is all well and good. (In fact, it’s perfunctory.) But the whole question here concerns the ‘fitness factors’. We’ve already determined that the ‘unicell’ form is ‘more fit’ than the ‘colonial form’ in nutrient uptake. We’ve determined that the ‘colonial’ form is ‘much more fit’ than the ‘unicell’ form for predation.

“More fit for predation?” That’s not how fitness works. Within a given environment, fitness is fitness. The colony is more resistant to predation, which contributes to its higher fitness in most environments where the predator is present.

You’ve assumed all along that a ‘mutation’ occurs. So we have 1 mutated cell. Not 1 mutated cell per ml., but 1 cell in the entire culture. (Remember, now, that you’ve made a big thing about the mutation ‘not being there before’.)

Which of course I didn’t. I “made a big thing” about the mutation not necessarily being there before. Blast seems to really really want us to say that the mutation either must have occurred before the flagellate was introduced, or that it must have occurred afterwards. But the truth is that both are possibilities; neither is ruled out by known data.

With that in mind, you have a culture which, after a ‘grazing down’ by the Ochromonus (5 days), is in a steady-state. BOTH the O. vallecias and the Chlorella are at 0.1 % of their maximum density. The initial density of the Chlorella was 2 x 10^6 cells/ml. For simplicity’s sake, let’s take 0.1 % of the initial density, which is 2 x 10^3 cells/ml.

Now, we have a steady-state situation. This means that both the Ochromonus and the Chlorella are going to maintain their levels: the ‘unicells’ keep multiplying and dividing, and the Ochromonus keeps on eating.

Remarkably enough, Blast doesn’t seem to know what a steady state is or how you get one. We know it’s not a steady state, because the Chlorella population rebounds immediately afterward, and we wouldn’t expect it to be a steady state because a two-species predator-prey system often doesn’t converge to one, instead oscillating indefinitely. As the paper says, “This reduction in predation pressure allowed the Chlorella population to recover and increase rapidly, in the manner of a classical predator-prey oscillation.”

Excluding chemical induction—which you insist on—then we have a situation in which there is a limited amount of nutrient, for which ONLY the ‘unicell’ and the ‘mutant morph’(= ‘colonial’ form) compete. Now, we’ve ALREADY established that the ‘unicells’ out compete (are ‘more fit’) the ‘colonial’ forms.

Er, no we didn’t. We established that the unicells aren’t fitter than the colonies when there’s predators about. You yourself said that “the ‘colonial’ form is ‘much more fit’ than the ‘unicell’ form for predation;” that’s rather garbled, but surely it implies that the colony’s fitter when there’s a strong predation pressure?

We also know that there are way more ‘unicell’ forms than ‘colonial’ forms. So “N” (the population size) is greater for the ‘unicells’; and “r” (the fitness factor) is greater for the ‘unicells’. So, tell me, what does Population Genetics 101 tell you is going to happen? The ONLY answer to that is that the ‘unicells’ are going to continue to out compete the ‘colonial form’, keeping it a very low level. So, then, where did the ‘colonial forms’ that were seen (and measured) in the experiment come from?

Blast continues to think that the initial dominance numbers-wise of unicells will have an effect on their steady-state population. Again, this is simply mathematically false. It will affect how fast they reach that steady state, but not what it actually is.

Let me just add: the ‘mutant morph’= ‘colonial form’, doesn’t ‘know’ that the Ochromonus is there. And the presence of the Ochromonus does not add fitness to the ‘colonial form’. Thus the analysis is no different than for the circumstances you just described.

Now this is very strange. Yes, the presence of Ochromonas doesn’t enhance the fitness of the colony…after all, it occasionally eats young colonies too. But it severely decreases the fitness of the unicell, and since it’s relative fitness that matters, obviously this leads to dominance of the colony.

But, of course, as I’ve pointed out above, it is a ‘fitness’ relative to predation, but NOT relative to nutrient uptake.

Again, this is meaningless. You can talk about contributions to relative fitness thanks to predation resistance or nutrient uptake superiority; you can’t talk about two separate kinds of fitness!

When the predator’s absent, unicells grow and reproduce faster than colonies. Unicells are fitter.

When the predator’s present and abundant, unicells still grow and reproduce faster than colonies, but now they also get eaten a lot, and so their net population growth rate is slower than the colonies’. Colonies are fitter.

When both predators and unicells are rare, unicells grow and reproduce faster than colonies, but also get eaten occasionally, so their net population growth rate is the same as the colonies’. Both morphs are equally fit.

If there’s a simpler way to put this, I don’t know it.

Blast continues to deny that allele frequency changes count as evolution:

Well, you’re dealing with me, Anton. Now, tell me, if you have one of those new screwdrivers which can be ‘shifted’ from one kind of tip to another, with ALL the tips in the meanwhile being inside of a canister that is part of the screwdriver, when you switch from one tip to another, has that screwdriver really changed? That is, is it a new ‘species’ of screwdriver each time you change the tip? How do you answer? I think you see the parallel to allelic frequency.

That analogy will be remotely applicable to evolutionary theory once screwdrivers start having babies.

And yes, of course every allele frequency change doesn’t produce speciation. This doesn’t change the fact that it’s an instance of evolution. Evolution includes more than just speciation—any undergrad bio major would know that.

Blast says strange things about plankton:

I’m very happy, Anton, that you think you’re closer to zooplankton than Chlorella is to zooplankton. Chlorella is a phytoplankton. It lives and resides in a similar environment to the zooplankton.

Huh. Mountain goats live and reside in a similar environment to fir trees. So do rocks. I guess that means they’re all closely related.

Given that “zooplankton” is a category that includes everything from protists to copepods to larval fish, of course we’re more closely related to some of them than Chlorella is. And, equally clearly, it’s very silly to say zooplankton in general “is related to” anything in particular.

Blast continues to misunderstand the statistics of mutations:

That’s right. During a ‘particular timespan’, the mutation rate approaches an average.

Aside from questions of exactly what you mean by “mutation rate approaches an average,” since that doesn’t mean nearly the same thing as “mutation rate is uniform”:

Again, it does this sometimes, in some particular parts of the genome, of some particular lineages. Often it doesn’t. Blast has no particular reason to assume mutation rates are uniform in the relevant parts of the Chlorella genome in this instance. Particularly because those parts are under heavy and varying selection pressures—which is what the experiment was designed to effect!

Moreover, as I explained before different kinds of mutations occur at different frequencies. For instance, deletions are more common than insertions. If a given deletion is responsible for a shift from unicell to colony, obviously a reverse shift via the appropriate insertion will tend to be less probable and will take longer to occur.

Now why—other than hand-waving—is the ‘reverse’ mutation that much slower than the ‘forward’ one? You say there’s all sorts of ways this ‘mutation’ can come about. Then why aren’t there a whole lot of ways for it to revert? It’s a significant weakness in the argument for mutation.

Why should there be a roughly equal number of ways for it to revert? It’s obviously quite possible that Phenotype X results from a relatively large number of genotypes, and Phenotype Y results from a smaller number.
And again, reproductive rate and culture size and timespan are as important to the overall likelihood of a reversion as the per-cell-division probability of an appropriate mutation. Fewer organisms, a younger culture or a slower reproductive rate obviously lower the chance of a given mutation popping up. Since we know the colonies have a lower reproductive rate in the absence of the predator, and since the colony cultures were years younger than the original culture, and since they were each founded with only one or a few colonies…well, there you go.

—-

So no, all told, it remains extremely unlikely that Blast ever pulled any sort of degree in biology. He seems to think my opinion in this regard makes me “arrogant,” which is odd. I mean, I probably am arrogant; that’s a fairly plausible character flaw of mine. But I’m well aware that the average bio grad student knows light-years more than I do on matters biological. It’s the fact that Blast doesn’t know the rudiments of this stuff that makes me doubt his claim.

Comment #85821

Posted by Anton Mates on March 10, 2006 4:47 PM (e)

Oh, and while I’m looking upthread, I notice that after—what’s it been, four months now?—Blast still hasn’t managed to answer the question posed to him over here: If organisms can’t evolve from one “kind” to another, as he claims, then does that mean Helacyton gartleri is the same kind as Homo sapiens or not?

His last response on that matter within this thread was that it’s “a stupid question.” Fair enough–no reason to expect Blast’s “kinds” concept to actually help us understand the observable world. That would be, as Dembski says, a “pathetic level of detail.”

Comment #85825

Posted by Anton Mates on March 10, 2006 5:00 PM (e)

Lest I sound like I’m on vendetta because the guy killed my dog, though, let me mention again that Blast did point out the probable error in the paper’s reported dilution rate. Props to him for that.

Comment #85834

Posted by Steviepinhead on March 10, 2006 5:48 PM (e)

Yeah. We should definitely give credit when credit is due:

Just because he takes completely idiotic positions, does not mean that Blast is a complete idiot.

Necessarily.

Though Lenny has several very creditable arguments that go the other way.

Comment #85885

Posted by BlastfromthePast on March 10, 2006 11:24 PM (e)

Anton, if you live in southern California, come by and I’ll show you my degree.

There’s another mistake in the paper–somewhat trivial, but there nonetheless.

He says that the ratio of mother cell membranes counted to the number of unicells is 1:4. He then says this means that 75% of the time there are two daughter cells, and 25% of the time there are four daughter cells. Write an equation for that, and there’s no solution except the trivial solution of zero. He should have said that ‘75% of the time the mother cell divides into four daughter cells, and that 25% of the time it divides into 8 daughter cells. The ratio then works out.

Anton, you have to understand that for me the Theory of Evolution is SO wrong that I have absolutely no motivation to learn it properly. Plus, when I say something, I’m giving the gist of an idea. I don’t plan on publishing what I write here, so the only thing that matters is the basic idea. And, yes, maybe I make it a bit difficult for you; but I guess I’m assuming you can get to the gist. Maybe that’s unfair on my part. But as I’m sure you know, we do have other things to do in life, and we can’t always take the time to get all the details right.

As to the 1.68, I misunderstood that as days/generation, rather than what it really is, generations/day, which Vicklund correctly points out is a little more than 14 hours per generation. The reason that they say 10-20 generations is that when there are multiple forms present in the culture variable growth rates can occur, with one form reproducing faster than another. So the authors were just hedging–which makes the range understandable.

One last go-round: if we take the 10 days–we’re told that even 100+-cells were present then–and subtract the 5 days (which is when my intuition tells me the signal should be felt), that leaves 5 days. This translates into 8 generations. 2^8th power is 256. So the ‘initial’ density of the ‘variant’ would be something like 1/500th (due to differential densities) or 1/1000th (also taking into account an additional day of reproduction) of the 0.1% ‘grazed down’ density of the ‘unicells’. I still think the numbers work out suggesting that “if” the ‘variant’ were there originally, that it would have somewhere, at sometime, been detected.

But, I think we’ve beaten this thing to death. And we all probably need a rest.

I hope somebody pursues this experiment.

Oh, BTW, when I wrote “slowly dissolving”, I was quoting by memory. I think they actually say the ‘colonies’ “slowly decline”, or something like that.

Comment #85896

Posted by Anton Mates on March 11, 2006 12:51 AM (e)

Posted by BlastfromthePast wrote:

Anton, if you live in southern California, come by and I’ll show you my degree.

God, I wish. I love my school, but magically enable me to complete my thesis in Cali instead of Ohio and you can have my degrees.

There’s another mistake in the paper—somewhat trivial, but there nonetheless.

He says that the ratio of mother cell membranes counted to the number of unicells is 1:4. He then says this means that 75% of the time there are two daughter cells, and 25% of the time there are four daughter cells. Write an equation for that, and there’s no solution except the trivial solution of zero. He should have said that ‘75% of the time the mother cell divides into four daughter cells, and that 25% of the time it divides into 8 daughter cells. The ratio then works out.

Actually, that wouldn’t work out either–the ratio would be 1:5 in that case. It does look like Boraas’ figures there are erroneous, but it’s impossible to work out what the true numbers should be from the ratio alone, since apparently the mother cell can divide into anywhere from 2-16 daughters. There’s an infinite number of daughter-number probability combos that would give you the ratio above.

Anton, you have to understand that for me the Theory of Evolution is SO wrong that I have absolutely no motivation to learn it properly.

Which seems very problematic to me. How do you overturn a theory without understanding it first? I’ve read assorted creationist/ID authors (and have checked Denton out of the library as per your advice) because I wanted to make sure they were wrong.

Plus, when I say something, I’m giving the gist of an idea. I don’t plan on publishing what I write here, so the only thing that matters is the basic idea. And, yes, maybe I make it a bit difficult for you; but I guess I’m assuming you can get to the gist. Maybe that’s unfair on my part. But as I’m sure you know, we do have other things to do in life, and we can’t always take the time to get all the details right.

True, but that’s why we have experts in each field–so they can get the details right. And you can’t really argue against them unless you can do the same.

As to the 1.68, I misunderstood that as days/generation, rather than what it really is, generations/day, which Vicklund correctly points out is a little more than 14 hours per generation. The reason that they say 10-20 generations is that when there are multiple forms present in the culture variable growth rates can occur, with one form reproducing faster than another. So the authors were just hedging—which makes the range understandable.

I believe Vicklund now agrees with me that there should be a ln(2) factor in there, producing the generation time of 9.9 hours. Have you an argument against?

And incidentally, I think the range of generation numbers given for various timespans (time from flagellate introduction to colony appearance, time from colony appearance to dominance, etc.) probably has as much to do with different data from different replicates of the experiment, as with the authors wanting to leave a margin of uncertainty.

One last go-round: if we take the 10 days—we’re told that even 100+-cells were present then—and subtract the 5 days (which is when my intuition tells me the signal should be felt), that leaves 5 days. This translates into 8 generations. 2^8th power is 256. So the ‘initial’ density of the ‘variant’ would be something like 1/500th (due to differential densities) or 1/1000th (also taking into account an additional day of reproduction) of the 0.1% ‘grazed down’ density of the ‘unicells’. I still think the numbers work out suggesting that “if” the ‘variant’ were there originally, that it would have somewhere, at sometime, been detected.

But the 10-day mark is the first time the colonies are even described. They aren’t described as dominating the population until around the 16-day mark:

“During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a)….During a second cycle of flagellate growth and Chlorella decline (16 days, Fig. 2a), the Chlorella colonies persisted while the Chlorella unicells declined to 1% of the total cells in the culture.”

Since there’s no indication that the colonies are particularly common at 10 days, there’s no reason to think that 5 days earlier (when as you mention they would have been rarer by two or three orders of magnitude) they would have been visible at all.

Beyond that, you’re arbitrarily chopping 5 days off the time from predator induction to colony appearance because of your hypothesized signal, which isn’t particularly relevant if we’re now considering the “pre-existing colonial morph gets selected for” model instead. The observed time was 10 days, not 5–a pre-existing variant could have been up to 1,000,000 times rarer at the time of introduction. (And likewise, even if only a single mutant colony arose after the introduction, its progeny could be present in the hundreds of thousands by the 10-day mark, hence easily visible.)

But, I think we’ve beaten this thing to death. And we all probably need a rest.

I hope somebody pursues this experiment.

It would be nice. Someday when I have a mansion and a four-hour workday I’ll park a few chemostats in the tearoom, next to the fishtanks where I farm those awesome inorganic living membranes Maselko & Strizhak found. I mean, these experiments can’t be hard, right?

Comment #85903

Posted by PvM on March 11, 2006 1:59 AM (e)

So let’s look at some of the data some more. Initially the ratio of unicell to multicell may have been 10000. After the initial decline the numbers seem to be about 10 to 1 assuming no reproduction of the multicell. But in 5 days 8 to 10 generations have passed or 2^8 to 2^10 or 256-1024 duplications of anywhere between 2 and 8 (16?) daughter cells. Seems that the numbers are hardly that unfavorable when compared to the actual data.

Blast wrote:

Anton, you have to understand that for me the Theory of Evolution is SO wrong that I have absolutely no motivation to learn it properly

That’s pretty shocking, you oppose something which you have failed to learn properly. Somehow that explains a lot.

So your claim that you had shown Boraas to be irrefutably wrong seems a bit premature now that more and more of your ‘arguments’ are shown to be erroneous?

What do you think Blast? Time to get some sneakers too?

Comment #85930

Posted by W. Kevin Vicklund on March 11, 2006 11:10 AM (e)

I still think the numbers work out suggesting that “if” the ‘variant’ were there originally, that it would have somewhere, at sometime, been detected.

As I said previously, IT WAS. In fact, the first person to demonstrate that he authors had encountered the variant several times over the course of 20 years of routine screenings was YOU!

blast, on Feb 27 in Comment #82422 wrote:

Sorry. From the paper: ” Initially, the culture tube was filled with medium and inoculated with Chlorella vulgaris Beij obtained from the University of Texas Culture Collection (UTEX #26). A steady state was established for the alga, which was then available as food to the flagellate predator. In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continuous cultures.”{emphasis removed)

Comment #85932

Posted by Russell on March 11, 2006 11:54 AM (e)

Blast wrote:

you have to understand that for me the Theory of Evolution is SO wrong that I have absolutely no motivation to learn it properly.

Say no more.

I mean really, say no more.

Comment #85935

Posted by Anton Mates on March 11, 2006 12:13 PM (e)

W. Kevin Vicklund wrote:

I still think the numbers work out suggesting that “if” the ‘variant’ were there originally, that it would have somewhere, at sometime, been detected.

As I said previously, IT WAS. In fact, the first person to demonstrate that he authors had encountered the variant several times over the course of 20 years of routine screenings was YOU!

Ah, but those were “loose clusters,” which are clearly qualitatively different from multicells, multicellular forms, colonies, and colonies (alternate meaning). Remember, if you believe in the concept of “synonyms,” the terrorists have already won.

Comment #86063

Posted by BlastfromthePast on March 12, 2006 3:05 PM (e)

Anton Mates wrote:

Actually, that wouldn’t work out either—the ratio would be 1:5 in that case. It does look like Boraas’ figures there are erroneous, but it’s impossible to work out what the true numbers should be from the ratio alone, since apparently the mother cell can divide into anywhere from 2-16 daughters. There’s an infinite number of daughter-number probability combos that would give you the ratio above.

Subtract out the four cells that were there at the beginning, and you have a ratio of 1 mother cell membrane to 4 new unicells. But, you’re right, if you say the mother cells can divide into 2 to 16 daughter cells, the 75% and 25% numbers are approximations at best.

Anton Mates wrote:

Which seems very problematic to me. How do you overturn a theory without understanding it first? I’ve read assorted creationist/ID authors (and have checked Denton out of the library as per your advice) because I wanted to make sure they were wrong.

When you’re dealing with ‘fitness’ and ‘selection pressure’ and that sort of stuff, the best refutation of those ideas comes from Fred Hoyle’s book.

I’m familiar with all the basic arguments. Remember, in the end, it’s really no more than RM+NS–which is not a complicated idea. I’ve only twice thrown down a book in disgust. Once was while I was reading the Orgins of Species. The other time was when I was reading Ernst Mayr’s “What’s Evolution” on the topic of ‘macroevolution’. Both times, I was completely flabbergasted at the lack of proper logic.

Look at the experiment at hand: the Chlorella and Ochromonus were in a steady-state condition for 7 months. How many Chlorella were produced if the 8-celled Chlorella was present at about the initial density of 2 x 10^6 cells/ml x 500 ml? Overall, that’s 1 x 10^9 cells that are being replace every 14+ hours x 210 days. That’s 3.6 x 10^12 Chlorella produced over that time period (rough approximation, of course). Well, what about the Ochromonus? There’s not too many unicells to eat–it’s at a reduced steady-state number, and yet there are all these 8-celled critters to chew on. Why not mutate? Let’s say it takes twice as long for it to reproduce; that still leaves 1.8 x 10^12 Ochromonus that are produced. 10^-8 is an average mutation rate that most scientists agree on (Boxhorn uses that figure in his Talks.Orign article). That’s a ‘per nucleotide’ number. Let’s assume that Ochromonus has 10^6 nucleotides that code (very conservative assumption). Then that means that there were 1.8 x 10^10 mutations that occurred in the Ochromonus during the 8 months experiment that they talk about in Fig 1a. 10 trillion mutations, and Ochromonus has no idea that a whole bunch of 8-celled critters are all around it. Why not? Why the stability? Why can we assume that the Chlorella ‘mutated’, but that for some reason the Ochromonus can’t?

I’ve heard this somewhere else; but here goes: “what’s good for the goose, is good for the gander.” Why is the theory one-sided?

The more you study biology, what becomes the most amazing is not that things change, but that they don’t change. It’s the stability that needs to be explained, not the instability.

Anton Mates wrote:

True, but that’s why we have experts in each field—so they can get the details right. And you can’t really argue against them unless you can do the same.

But I do follow their arguments. But what are the arguments for macroevolution? That finches beaks change size and that dark moths become light moths? I haven’t yet found a convincing argument

Anton Mates wrote:

I believe Vicklund now agrees with me that there should be a ln(2) factor in there, producing the generation time of 9.9 hours. Have you an argument against?

My argument would be that Boxhorn says “the critters are growing exponetially with their growth rate being the dilution rate (in flow of medium/bottle volume) of the system.”

He doesn’t say their “exponential growth rate” is the “dilution rate”, but that they’re “growth rate” is equal to the “dilution rate”. Remember it’s ‘steady-state’ conditions he’s talking about, and ‘steady-state’ and ‘exponential growth’ are contradictory. At just the right inflow of nutrient and outflow of critters and stuff, equal ‘densities’ are seen. So I would interpret it to mean that the growth rate is so much per day–some constant that is related to the inflow rate.

I’ve really got to go. I’ll post more as time permits.

Comment #86067

Posted by PvM on March 12, 2006 3:29 PM (e)

Let’s look—once again—to the ‘big picture’: In the ‘beginning’, there are mother cells, daughter cells, and mother cell walls. In the ‘end’, there are mother cells, daughter cells, and mother cell walls. So, tell me, what has ‘evolved’? It appears that the cell membranes of the unicells have become more sticky. Is it a ‘chemical’ response? I think so. Something has ‘changed’; but nothing has ‘evolved’. (Please don’t bore me with an argument that wants to equate the two. Thank you.)

Yes, let’s not ‘bore’ Blast with the facts now shall we.

Comment #86071

Posted by PvM on March 12, 2006 3:50 PM (e)

Blast wrote:

Look at the experiment at hand: the Chlorella and Ochromonus were in a steady-state condition for 7 months. How many Chlorella were produced if the 8-celled Chlorella was present at about the initial density of 2 x 10^6 cells/ml x 500 ml? Overall, that’s 1 x 10^9 cells that are being replace every 14+ hours x 210 days. That’s 3.6 x 10^12 Chlorella produced over that time period (rough approximation, of course). Well, what about the Ochromonus? There’s not too many unicells to eat—it’s at a reduced steady-state number, and yet there are all these 8-celled critters to chew on. Why not mutate?

Yes, why not mutate… But sadly enough that’s not really how evolution works. While mutations happen quite continuously, finding a mutation which helps deal with the large source of untapped foods may be quite a difference. And realize that once it manages to mutate into being able to eat the 8 cell one, the chlorella colony size will trivially increase.

Let’s say it takes twice as long for it to reproduce; that still leaves 1.8 x 10^12 Ochromonus that are produced. 10^-8 is an average mutation rate that most scientists agree on (Boxhorn uses that figure in his Talks.Orign article). That’s a ‘per nucleotide’ number. Let’s assume that Ochromonus has 10^6 nucleotides that code (very conservative assumption). Then that means that there were 1.8 x 10^10 mutations that occurred in the Ochromonus during the 8 months experiment that they talk about in Fig 1a. 10 trillion mutations, and Ochromonus has no idea that a whole bunch of 8-celled critters are all around it.

That’s just not how mutations work.

Why not? Why the stability? Why can we assume that the Chlorella ‘mutated’, but that for some reason the Ochromonus can’t?

We don’t. We observe that the original stock contains the occasional variant genetic multicellular/multicolonial form.

I’ve heard this somewhere else; but here goes: “what’s good for the goose, is good for the gander.” Why is the theory one-sided?

It isn’t. It’s not the theory which is the issue here but rather your limited understanding of evolutionary theory. This is not meant as an ad hominem but rather as an explanation. You yourself have said that your interest and understanding of evolutionary theory in this area may be lacking.

Blast wrote:

you have to understand that for me the Theory of Evolution is SO wrong that I have absolutely no motivation to learn it properly.

Comment #86072

Posted by PvM on March 12, 2006 4:01 PM (e)

Blast wrote:

The more you study biology, what becomes the most amazing is not that things change, but that they don’t change. It’s the stability that needs to be explained, not the instability.

Aha, welcome to evolutionary theory. Now let’s see if I can provide you with an introductory overview of the difference between phenotypic and genotypic variation as well as the concept of neutrality.

Take aways:

1. While the phenotype can remain in stasis, the genotype can ‘evolve’
2. There exist extensive neutral or near-neutral pathways in the genome
3. In instances of phenotype stasis, the genotype ‘evolves’ very similar to the concept of diffusion.
4. Occasionally a non-neutral mutation arises which gives rise to an improved fitness and may be selected for.

There is some excellent work done on these topics by such people as Peter Schuster, Walter Fontana, Stadler, Toussaint and many others.
Hope this helps. If you are still interested, I can provide you with some very fascinating links

search for: evolvability, neutrality, scale free networks, RNA networks

Comment #86134

Posted by Anton Mates on March 12, 2006 7:32 PM (e)

BlastfromthePast wrote:

Actually, that wouldn’t work out either—the ratio would be 1:5 in that case. It does look like Boraas’ figures there are erroneous, but it’s impossible to work out what the true numbers should be from the ratio alone, since apparently the mother cell can divide into anywhere from 2-16 daughters. There’s an infinite number of daughter-number probability combos that would give you the ratio above.

Subtract out the four cells that were there at the beginning, and you have a ratio of 1 mother cell membrane to 4 new unicells.

Why would you subtract anything? The original four cells aren’t there anymore anyway, but they each left a maternal membrane behind and their daughters–using your numbers–number 3*4 + 1*8 = 20, so the ratio’s still 1:5.

When you’re dealing with ‘fitness’ and ‘selection pressure’ and that sort of stuff, the best refutation of those ideas comes from Fred Hoyle’s book.

Given that that’s nowhere near Hoyle’s area of expertise and I’ve seen excerpts of that book that involve very very bad math, I’m skeptical. But I’ll read it.

I’m familiar with all the basic arguments. Remember, in the end, it’s really no more than RM+NS—which is not a complicated idea. I’ve only twice thrown down a book in disgust. Once was while I was reading the Orgins of Species. The other time was when I was reading Ernst Mayr’s “What’s Evolution” on the topic of ‘macroevolution’. Both times, I was completely flabbergasted at the lack of proper logic.

I’ve never read that particular work of Mayr’s, but I take issue with plenty of things he’s written. But surely you realize that your reaction to the Origin is very different from the reactions of a huge number of initially skeptical scientists? Whatever defects it has–and it has some, no doubt–a “flabbergasting lack of logic” is not one of them.

Look at the experiment at hand: the Chlorella and Ochromonus were in a steady-state condition for 7 months. How many Chlorella were produced if the 8-celled Chlorella was present at about the initial density of 2 x 10^6 cells/ml x 500 ml? Overall, that’s 1 x 10^9 cells that are being replace every 14+ hours x 210 days. That’s 3.6 x 10^12 Chlorella produced over that time period (rough approximation, of course). Well, what about the Ochromonus? There’s not too many unicells to eat—it’s at a reduced steady-state number, and yet there are all these 8-celled critters to chew on. Why not mutate? Let’s say it takes twice as long for it to reproduce; that still leaves 1.8 x 10^12 Ochromonus that are produced.

Problem with that: the Ochromonas population density at steady-state is about a thousandth of the observed maximum which occurred early on. And from what I can see in figure 2 (plus the fact that O. vallescia is an obligate phagotroph “which requires a constant supply of food,” so it can only multiply as far as the initial supply of Chlorella permits) it’s unlikely that that maximum was anywhere near Chlorella’s max. So there’d be several orders of magnitude fewer Ochromonas produced than you estimate.

10^-8 is an average mutation rate that most scientists agree on (Boxhorn uses that figure in his Talks.Orign article). That’s a ‘per nucleotide’ number. Let’s assume that Ochromonus has 10^6 nucleotides that code (very conservative assumption). Then that means that there were 1.8 x 10^10 mutations that occurred in the Ochromonus during the 8 months experiment that they talk about in Fig 1a. 10 trillion mutations, and Ochromonus has no idea that a whole bunch of 8-celled critters are all around it. Why not? Why the stability? Why can we assume that the Chlorella ‘mutated’, but that for some reason the Ochromonus can’t?

Who’s assuming? Ochromonas didn’t change its size preference over the period it was observed, by mutations or any other mechanism. This is only a “problem” for evolutionary theory if you assume it should change that fast. Now if you show via other research that there are a large number of highly probable mutations that would change the size preference as necessary, without harmful side-effects that would reduce Ochromonas’ overall fitness, and that at least one of these is likely to occur in the given timespan, then it’d be reasonable to ask why this didn’t happen. But you haven’t done that.

The more you study biology, what becomes the most amazing is not that things change, but that they don’t change. It’s the stability that needs to be explained, not the instability.

It’s rather odd that you say that when you’ve previously provided various arguments in favor of stability. Specific mutations highly improbable and need a long time to appear, yes? Most mutations harmful or neutral, yes?

How did we get from “evolutionary changes are implausibly fast” to “evolutionary changes are implausibly slow?”

I believe Vicklund now agrees with me that there should be a ln(2) factor in there, producing the generation time of 9.9 hours. Have you an argument against?

My argument would be that Boxhorn says “the critters are growing exponentially with their growth rate being the dilution rate (in flow of medium/bottle volume) of the system.”

He doesn’t say their “exponential growth rate” is the “dilution rate”, but that they’re “growth rate” is equal to the “dilution rate”. Remember it’s ‘steady-state’ conditions he’s talking about, and ‘steady-state’ and ‘exponential growth’ are contradictory.

This is incidental, but they’re not contradictory at all. A chemostat is designed to have a steady state that permits exponential growth. The net population increase is zero, sure, because of organism loss from medium cycling, but the organisms don’t know that. They’re still reproducing at a constant rate relative to their current population, which defines exponential growth.

At just the right inflow of nutrient and outflow of critters and stuff, equal ‘densities’ are seen. So I would interpret it to mean that the growth rate is so much per day—some constant that is related to the inflow rate.

I think that’s how we’re all interpreting it. But the ln(2) comes not from the definition of the growth rate, but from how you get the generation time once you have the growth rate.

A growth rate of k implies a population of size A exp(k*t) for some constant A. If you assume “generation time” to be the same as “doubling time,” as we did, then the timespan necessary for that population to double is simply ln(2)/k.

Boxhorn, I think, instead defined the generation time as “average lifespan of an organism within the population.” Which for all I know may be the best way to do it for a ton of applications, but probably isn’t if you’re trying to calculate a population-wide mutation rate.

Comment #86412

Posted by BlastfromthePast on March 14, 2006 8:21 PM (e)

Blast wrote:

you have to understand that for me the Theory of Evolution is SO that I have absolutely no motivation to learn it properly.

Since you are all so quick to pounce on this statement, let me restate it: “I have absolutely no motivation to learn the theory with exactitude.” This is a more accurate rendering of what I intended to say in the first place, and should slow down the incessant peanut gallery.

Correction aside, let me segue to the following:

PvM wrote:

Aha, welcome to evolutionary theory. Now let’s see if I can provide you with an introductory overview of the difference between phenotypic and genotypic variation as well as the concept of neutrality.

Take aways:

1. While the phenotype can remain in stasis, the genotype can ‘evolve’
2. There exist extensive neutral or near-neutral pathways in the genome
3. In instances of phenotype stasis, the genotype ‘evolves’ very similar to the concept of diffusion.
4. Occasionally a non-neutral mutation arises which gives rise to an improved fitness and may be selected for.

Pim, I have no problem understanding this ‘theory’ at all–I was quite adept at Chemistry; and I took Biochemistry as a grad student. The problem is not understanding the theory. The problem is I don’t find the theory believable! That’s the problem. From an intuitive sense, the law of probabilites doesn’t make the theory credible. I’ve looked all over for a credible argument, and have not found it. To me, the emporer has no clothes.

Anton Mates wrote:

But surely you realize that your reaction to the Origin is very different from the reactions of a huge number of initially skeptical scientists? Whatever defects it has—and it has some, no doubt—a “flabbergasting lack of logic” is not one of them.

Well, when Darwin suggests that “varieties give rise to species, and species to genera, and genera to families, and families to orders”, well, then, that’s just plain, old ‘poppycock’. He’s standing the Linnean Classification system on its head–which is contrary to human experience–and in the process guilty of a “flabbergasting lack of logic.” What else can I say. But he has a whole lot of other whoppers. That doesn’t completely undermine what he has done, nor displace him from scientific prominence; but, nonetheless, I’d put a lot of what he wrote in the same category as Lamarck. (In fact, there are those who argue that Lamarck deserves a higher rank in the constellation of evolutionary thinkers. I’ll let them fight that one out.)

Anton Mates wrote:

Who’s assuming? Ochromonas didn’t change its size preference over the period it was observed, by mutations or any other mechanism. This is only a “problem” for evolutionary theory if you assume it should change that fast.

This is the kind of statement that–from my vantage point–makes RM+NS ‘unfalsifiable.’ If something appears to mutate: “Look, lo and behold, an example of ‘evolution’.” And it it doesn’t mutate: “Well, why in the world would you expect it to mutate?”

Let’s not get bogged down with this; but at least try and see how these ‘explanations’ look to someone who believes neo-Darwinism is, well, “illogical.”

Anton Mates wrote:

It’s rather odd that you say that when you’ve previously provided various arguments in favor of stability. Specific mutations highly improbable and need a long time to appear, yes? Most mutations harmful or neutral, yes?

How did we get from “evolutionary changes are implausibly fast” to “evolutionary changes are implausibly slow?”

The “implausibly fast” argument was a mathematical argument. The “implausibly slow” argument simply takes note of the fossil record (species appear, remain constant, and then disappear=stasis), the repair mechanisms of eukaryotic cells, and the stability posited by Mendelian genetics (the Hardy-Weinberg Law). We know mutations take place–all the time. And, yet, species stay the same. How come?

Anton Mates wrote:

A growth rate of k implies a population of size A exp(k*t) for some constant A. If you assume “generation time” to be the same as “doubling time,” as we did, then the timespan necessary for that population to double is simply ln(2)/k.

Correct me if I’m wrong, but I think the proper formula would be something like (A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G, where A = the amount of Chlorella at t=0, w = the rate at which pefectly fit Chlorella are ‘washed out’ (go flying over the edge of the chemostat), w’ is the amount of A washed out at t=0, g = the number of Chlorella that are being ‘eaten’/hour (grazed) by the Ochromonus, g’ the amount of A grazed at t=0 and G is some ‘constant’ growth rate. (And, yes, A-w’-g’ can become a new constant A’–just as long as we take note of what “A’” is.) Taking the natural log of both sides yields: ln (A-g’-w’)x k*t - ln (g*t + w*t) = ln G

From this we can get:

ln (A-g’-w’)xk*t - ln [t(g+w)] = ln G

ln (A-g’-w’)k*t/ln [t(g+w)] = ln G

ln [(A-g’-w’)kt/t(g+w)] = ln G

Raising this equation by the power of “e”, we get:

(A-g’-w’)kt/t(g+w) = G

The “t”’s cancel on the left side. So,

G = (A-g’-w’)k/(g+w)

A, g’, and w’are all constants. k, g, and w are all assumed to be ‘constant’ rates. Hence,

G = Constant = growth rate. The ‘time’ has dropped out of this equation, so there’s no longer an exp(t) term anymore. It’s no longer time-dependent

Hope all the above is right.

Anton Mates wrote:

Why would you subtract anything? The original four cells aren’t there anymore anyway, but they each left a maternal membrane behind and their daughters—using your numbers—number 3*4 + 1*8 = 20, so the ratio’s still 1:5.

Remember that I’m just trying to make sense of what Boraas, et.al. have written. However, it seems to me that their thinking goes like this: you have 4 ‘unicells’. This 4 ‘unicells’ become ‘mother cells’. 3 of these 4 ‘mother cells’ divide once (now there’s two cells), and then again (now there’s four cells). For each of these 3 ‘mother cells’, there are “3” NEW cells formed. (For a total of “9” new cells). The other ‘mother cell’ divides to form 2 cells; these divide to form 4 cells; and these in turn divide to form 8 cells. From this “1” ‘mother cell’, there are 7 ‘new’ ‘unicells’(The total is now 7 + 9 = 16). The 4 ‘mother cells’ produce 4 ‘mother cell membranes’. The ratio is then 4 ‘mother cell membranes’ to 16 ‘new cells’, or 1:4.

Now while I’m at it–in regards to what Pim has written and argued, and what Vicklund argues as well–this ratio of ‘mother cell membranes’ to new ‘unicells’ works in favor of my argument.

Let’s look at it this way: Pim and Vicklund argue that the ‘mutant’ strain was there from the beginning. So, at the beginning, we have ‘unicell’ Chlorella and ‘mother cell walls’ in the ratio of 1:4, and the ‘mutant strain’ of Chlorella. That means that if you took a ‘cell sample’ of 300-500 cells, you should also see–ad principio–roughly 75-125 ‘mother cell membranes.’ (I argue that you should also see the ‘mutant strain’ at the beginning; some of you disagree [Pim], or agree [Vicklund] with this.) If the idea is that once the Ochromonus is introduced then the ‘mutant strain’ has an advantage over the ‘unicells’ because they can’t be ‘preyed upon’, and that, as a result, the ‘mutant strain’ will increase in numbers and the ‘unicells’ will decrease, then the ‘million-dollar question’ is….…….(drum-roll once again)……what happens to the ‘mother cell membranes’?

According to your theory, since the ‘unicells’ continue to be produced, then the ‘mother cell walls’ would continue to be produced in a 1:4 ratio. At steady state, the Chlorella is at 0.1% of the 2 x 10^6 cells/ml density. So the ‘cell walls’ should amount to 5 x 10^5 walls/ml. Why aren’t they seen?

If, as I argue, we’re dealing with ‘chemical induction’, then it is a simple matter to say–in fact, didn’t someone recently quote me on this–that the ‘cell walls’ have become more sticky, and that the ‘cell walls’ now simply enclose the ‘daughter cells’; hence NO ‘mother cell walls.’

So, again, where did the ‘mother cell walls’ go?

Comment #86436

Posted by Steviepinhead on March 14, 2006 10:03 PM (e)

Wheeze on his Knees:

So, again, where did the ‘mother cell walls’ go?

Like the Mother Ship, they must have blasted through the wormhole into the Nth Dimension where the Great and Omnipotent Oz waves his wand over multitudes of munchkins and all the wittle cweeationists can hold hands and hope nobody ever finds any more fossils…or genomes…or instances of speciation…or mutations…or effects of selection…

Comment #86461

Posted by PvM on March 15, 2006 12:26 AM (e)

Blast wrote:

Since you are all so quick to pounce on this statement, let me restate it: “I have absolutely no motivation to learn the theory with exactitude.” This is a more accurate rendering of what I intended to say in the first place, and should slow down the incessant peanut gallery.

Let’s see

Blast wrote:

Pim, I have no problem understanding this ‘theory’ at all—I was quite adept at Chemistry; and I took Biochemistry as a grad student. The problem is not understanding the theory. The problem is I don’t find the theory believable! That’s the problem. From an intuitive sense, the law of probabilites doesn’t make the theory credible. I’ve looked all over for a credible argument, and have not found it. To me, the emporer has no clothes.

So the problem is you not really the theory. Argument from personal disbelief somehow does not really impress me. In fact, I doubt that you have looked all over for a credible argument, especially given your former statement about learning the theory. Look Blast, I understand, it may be hard to admit that you are wrong especially since you seem to have rejected evolutionary theory based on your ‘disbelief’. And yet when people try to educate you beyond your strawman understanding of said theory, and correct your arguments time after time, you seem to be unwilling to accept that you were wrong.

I have seen much of the same behavior amongst young earth creationists.

According to your theory, since the ‘unicells’ continue to be produced, then the ‘mother cell walls’ would continue to be produced in a 1:4 ratio. At steady state, the Chlorella is at 0.1% of the 2 x 10^6 cells/ml density. So the ‘cell walls’ should amount to 5 x 10^5 walls/ml. Why aren’t they seen?

Sigh… So many problems first of all the density is now at 1/1000th the original density. If they are hard to detect at the full density why do you believe that at much lower densities they should be more visible.

Of course, this argument does not help you, in either instance there are these unicells which divide and motherwalls should be formed. But your assumption about how many mother walls should be found needs to establish how many mother walls are to be expected and then you have to show that under your scenario this is better explained.

So far your argument seems mostly to be one of irrelevance. Does this mean that you have given up on your other irrefutable evidences? Look you have presented no evidence that these mother cells are ‘gone’, they are just present at much much lower concentrations.

Geez Blast, do the math.

Comment #86463

Posted by PvM on March 15, 2006 12:35 AM (e)

The “implausibly fast” argument was a mathematical argument. The “implausibly slow” argument simply takes note of the fossil record (species appear, remain constant, and then disappear=stasis), the repair mechanisms of eukaryotic cells, and the stability posited by Mendelian genetics (the Hardy-Weinberg Law). We know mutations take place—all the time. And, yet, species stay the same. How come?

If we explained would you care to listen or merely reject this as not very believable to you? Do you even know what the fossil record really looks like? Are you even willing to learn?

Lesson 1: Most mutations are neutral
Lesson 2: Do you understand speciation?

You do understand the difference between genetic and phenotypic variation?
Look Blast, if you do not care to educate yourself about evolutionary theory then why should we take your strawmen seriously?

Well, when Darwin suggests that “varieties give rise to species, and species to genera, and genera to families, and families to orders”, well, then, that’s just plain, old ‘poppycock’. He’s standing the Linnean Classification system on its head—which is contrary to human experience—and in the process guilty of a “flabbergasting lack of logic.” What else can I say.

Could you explain? This sounds like yet another common creationist confusion about what Darwin said, and what Linnean classification is all about. I’d love to hear your argument especially since the data that explain the flaws in your argument are quite simple to find.

Battson and other critics of macroevolution interpret this apparent “top-down” pattern as contrary to expectations from evolutionary theory. However, this pattern is generated by the way in which species are assigned to higher taxa. When a hierarchical classification is applied retrospectively to a diversifying evolutionary tree, a “top-down” pattern will of necessity result. Consider, for example, species belonging to a single evolving lineage given genus-level status. This genus is then grouped with other closely related lineages into a family. The common ancestors of these genera are by definition included within that family. Those ancestors must logically be older than any of the other species within the family. Thus the family level taxon would appear in the fossil record before most of the genera and species included within it. The “top-down” pattern of taxa appearance is therefore entirely consistent with a branching tree of life.

http://www.asa3.org/ASA/topics/Evolution/PSCF12-…

Hope this helps

Comment #86465

Posted by W. Kevin Vicklund on March 15, 2006 12:43 AM (e)

If nothing else, I have objections to the non-standard conventions you are using in your equations (for example, w’ should be rate and w(0) should be amount at t=0). Your equations look wrong to me, but I’m going to investigate further and attempt to address it in a different post.

Remember that I’m just trying to make sense of what Boraas, et.al. have written. However, it seems to me that their thinking goes like this: you have 4 ‘unicells’. This 4 ‘unicells’ become ‘mother cells’. 3 of these 4 ‘mother cells’ divide once (now there’s two cells), and then again (now there’s four cells). For each of these 3 ‘mother cells’, there are “3” NEW cells formed. (For a total of “9” new cells). The other ‘mother cell’ divides to form 2 cells; these divide to form 4 cells; and these in turn divide to form 8 cells. From this “1” ‘mother cell’, there are 7 ‘new’ ‘unicells’(The total is now 7 + 9 = 16). The 4 ‘mother cells’ produce 4 ‘mother cell membranes’. The ratio is then 4 ‘mother cell membranes’ to 16 ‘new cells’, or 1:4.

Unfortunately, your definition of “new cells” doesn’t match the conventions biologists use, and specifically don’t coincide with the specific case. When a Chlorella cell divides, it undergoes one or more cell divisions, after which the mother cell wall bursts and the daughter cells disperse, leaving an empty mother cell wall. It is impossible (and meaningless) to distinguish which of the daughter cells was the mother cell, and the article states that the ratio of empty cell walls to cells is about 1:4. I have a different solution to the problem. If 75% of the time the original divided into 2 cells, and 25% of the time it divided into 4 or more cells (approximately evenly distributed between 4, 8, and 16), then the ratio works out to about 1:4. If, of 25 originals cells, 19 cells begat two daughter cells, 2 begat 4 cells, 2 begat eight, and 2 begat sixteen, we would have a ratio of 25:(38+8+16+32) = 25:94 = 1:3.76 ~ 1:4. Does this make sense?

Now while I’m at it—in regards to what Pim has written and argued, and what Vicklund argues as well—this ratio of ‘mother cell membranes’ to new ‘unicells’ works in favor of my argument.

Polite request: could you refer to me as Kevin? It feels like you’re talking to my father (RIH) when you address me as Vicklund. But that is merely a personal preference on my part and has nothing to do with the discussion.

Let’s look at it this way: Pim and Vicklund argue that the ‘mutant’ strain was there from the beginning. So, at the beginning, we have ‘unicell’ Chlorella and ‘mother cell walls’ in the ratio of 1:4, and the ‘mutant strain’ of Chlorella. That means that if you took a ‘cell sample’ of 300-500 cells, you should also see—ad principio—roughly 75-125 ‘mother cell membranes.’ (I argue that you should also see the ‘mutant strain’ at the beginning; some of you disagree [Pim], or agree [Vicklund] with this.) If the idea is that once the Ochromonus is introduced then the ‘mutant strain’ has an advantage over the ‘unicells’ because they can’t be ‘preyed upon’, and that, as a result, the ‘mutant strain’ will increase in numbers and the ‘unicells’ will decrease, then the ‘million-dollar question’ is….…….(drum-roll once again)……what happens to the ‘mother cell membranes’?

More precisely, I pointed out that it has been noted in the past with as rare mutant and has been observed at a rate consistent with it being present at .1% concentration. I have not asserted that it actually was present in the culture at the beginning of the experiments in which colonies arose. I am willing to entertain the idea that the mutation is simple and accessible from the unicellular state and merely has been seen to arise spontaneously in detectable amounts several times a year. If it was present at the start, only on rare occurrences should we expect to see it at t=0 (about once every 25 replicates of the experiment). As the concentration of unicells decrease, so will the concentration of the empty mother cell membranes. This is because the colonies do not appear to cast off the mother cell membrane - they remain ‘stuck’ to it.

According to your theory, since the ‘unicells’ continue to be produced, then the ‘mother cell walls’ would continue to be produced in a 1:4 ratio. At steady state, the Chlorella is at 0.1% of the 2 x 10^6 cells/ml density. So the ‘cell walls’ should amount to 5 x 10^5 walls/ml. Why aren’t they seen?

Um, check your math. If the initial density is 2 x 10^6 cells/ml, then the steady-state density of unicell Chlorella should be 2 x 10^3 cells/ml. Given that the empty cell walls should be at a 1:4 ratio, this equals a density of 5 x 10^2 walls/ml. At the sample sizes implied earlier (300-500 cells at a density of 2 x 10^6 cells/ml), that’s less than one cell wall per sample!

Are you by chance forgetting that the empty cell walls will be washed out of the chemostat?

If, as I argue, we’re dealing with ‘chemical induction’, then it is a simple matter to say—in fact, didn’t someone recently quote me on this—that the ‘cell walls’ have become more sticky, and that the ‘cell walls’ now simply enclose the ‘daughter cells’; hence NO ‘mother cell walls.’

So, again, where did the ‘mother cell walls’ go?

Your prediction of sticky cell walls could have been cribbed directly from the paper (rhetorically speaking - I’m not accusing you of plagiarism, blast). The evolutionary explanation for the formation of colonies, quoted from the third paragraph under the heading Discussion:

Boraas wrote:

The most probable initial mechanism for colony formation, adhesion of the daughter cells to the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies (Fig. 1d) and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation).

Where did the mother cell walls go? They remain as part of the colony. Your prediction wrt the “stickiness” of the mother cell walls is exactly the same as the evolutionary prediction, except with a different cause. Again, I fail to see how the data withheld on empty mother cell walls would support your hypothesis and simultaneously discredit the evolutionary hypothesis. Both require the same data (again, wrt empty cell walls). Do you understand yet?

Comment #86482

Posted by Anton Mates on March 15, 2006 2:16 AM (e)

BlastfromthePast wrote:

Correct me if I’m wrong, but I think the proper formula would be something like (A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G, where A = the amount of Chlorella at t=0, w = the rate at which pefectly fit Chlorella are ‘washed out’ (go flying over the edge of the chemostat), w’ is the amount of A washed out at t=0, g = the number of Chlorella that are being ‘eaten’/hour (grazed) by the Ochromonus, g’ the amount of A grazed at t=0 and G is some ‘constant’ growth rate. (And, yes, A-w’-g’ can become a new constant A’—just as long as we take note of what “A’” is.) Taking the natural log of both sides yields: ln (A-g’-w’)x k*t - ln (g*t + w*t) = ln G

From this we can get:

ln (A-g’-w’)xk*t - ln [t(g+w)] = ln G

ln (A-g’-w’)k*t/ln [t(g+w)] = ln G

ln [(A-g’-w’)kt/t(g+w)] = ln G

Raising this equation by the power of “e”, we get:

(A-g’-w’)kt/t(g+w) = G

The “t”’s cancel on the left side. So,

G = (A-g’-w’)k/(g+w)

A, g’, and w’are all constants. k, g, and w are all assumed to be ‘constant’ rates. Hence,

G = Constant = growth rate. The ‘time’ has dropped out of this equation, so there’s no longer an exp(t) term anymore. It’s no longer time-dependent

Hope all the above is right.

Agh! No, sorry, that’s gibberish. I’ve got to finish a final exam over the next couple of days but after that I’ll do a derivation of the formulas for exponential growth (and chemostat growth) if no one else does.

Short answer, all those constants you threw in are irrelevant to the question of steady-state generation times. Either they’re not involved in steady-state or their effect is already rolled into A or k.

Comment #86516

Posted by Anton Mates on March 15, 2006 9:21 AM (e)

Oh, but before I do anything else–Kevin & Blast, you were right (as was Boxhorn, unsurprisingly) and I was wrong. No ln(2) in the formula for (predatorless) steady-state generation time. If the total population was literally increasing exponentially, you’d need that factor, but it’s unnecessary here. So Kevin’s estimate of 14 hours should be on the money. (But, as previously noted, that generation time will be shorter for any approximate steady-state in the presence of a predator, as was the case with Chlorella after the flagellate’s introduction.)

Comment #86531

Posted by David Wilson on March 15, 2006 10:14 AM (e)

In comment #81991

BlastfromthePast wrote:

As a mathematician, I don’t see how you can think Darwinism works.

But in comment #86412 he produced the following “calculation”:

Correct me if I’m wrong, but I think the proper formula would be something like (A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G, where A = the amount of Chlorella at t=0, w = the rate at which pefectly fit Chlorella are ‘washed out’ (go flying over the edge of the chemostat), w’ is the amount of A washed out at t=0, g = the number of Chlorella that are being ‘eaten’/hour (grazed) by the Ochromonus, g’ the amount of A grazed at t=0 and G is some ‘constant’ growth rate. (And, yes, A-w’-g’ can become a new constant A’—just as long as we take note of what “A’” is.) Taking the natural log of both sides yields: ln (A-g’-w’)x k*t - ln (g*t + w*t) = ln G

In his application of the logarithm to obtain the left side of the last equation Mr Blast has committed at least two elementary blunders which anyone with a sound grasp of high-school mathematics (let alone someone claiming to be a “mathematician”) never should have.

He then continues (equation nubers added by me):

From this we can get:

ln (A-g’-w’)xk*t - ln [t(g+w)] = ln G      [1]

ln (A-g’-w’)k*t/ln [t(g+w)] = ln G      [2]

The apparent claim that equation [2] follows from any of the preceding calculations is another elementary blunder.

ln [(A-g’-w’)kt/t(g+w)] = ln G

If this is supposed to be a consequence of equation [2] then that supposition is yet another elementary blunder. However, it so happens that this one cancels out the error introduced by the immediately preceding one, since this last equation does in fact follow from equation [1] (though it certainly doesn’t follow from the original equation, (A-w’-g’)exp(k*t)- w*t - g*t = G).

Draw your own conclusions.

Comment #86538

Posted by W. Kevin Vicklund on March 15, 2006 10:37 AM (e)

Well, it’s a good thing I previewed. It changes my post a bit.

I have modified blast’s definitions slightly for accuracy and convention.

A = amount of Chlorella cells
w = amount of cells being washed out
g = amount of cells being grazed
k = doubling rate
w’ = rate of cells being washed out
g’ = rate of cells being grazed
F = flow rate

What we should find is that terms on the left should either be all linear or all exponential. So we should see

Aekt-wew’t-geg’t=F

or something like that if it were exponential. This is a simplification of the real equation, which I have yet to derive, so it is not necessarily correct. The actual underlying equations are a set of four linked differential equations, one for the flow and one for each of the populations, that must be solved simultaneously. Not the easiest task in the world, no?

Anyway, unless people really want to see four complicated differential equations solved simultaneously, I think we can call the point moot. The take-home is that for steady-state only the generation time is inversely proportional to the growth rate (whether or not ln(2) is included, it is still inversely proportional), and the growth rate is equal to the flow rate (in non-predator chemostats) or greater than the flow rate (in predator chemostats). During the initial stages of the experiment (once the predator is introduced), the growth rate will exceed the flow rate, which means the generation time of the unicells will be less than the steady-state value of 14 hours during the first 20 days. The data I have seen from googling suggests the maximum possible doubling time for Chlorella is somewhere around 8 to 9 hours.

Comment #86612

Posted by Anton Mates on March 15, 2006 3:40 PM (e)

David Wilson wrote:

In his application of the logarithm to obtain the left side of the last equation Mr Blast has committed at least two elementary blunders which anyone with a sound grasp of high-school mathematics (let alone someone claiming to be a “mathematician”) never should have.

In his defense, when Blast said “As a mathematician…”, I believe he was referring to me, not him. (I don’t know if I should count as a mathematician yet, but I’m a math grad. Actually, screw it, if Dembski gets to call himself a mathematician, then I’m a mathematician too, and so’s my little sister in high school.)

Comment #86716

Posted by BlastfromthePast on March 16, 2006 12:03 AM (e)

PvM wrote:

So the problem is you not really the theory. Argument from personal disbelief somehow does not really impress me.

Argument from personal belief somehow doesn’t impress me either. The “Origins” is filled with “I believe”, “I have no doubt”, etc., etc.

The problem with the theory is–since it seems impossible for any of you to understand plain English–it doesn’t add up. It’s highly improbable–like winning the lottery every week for 100 years; that improbable.

PvM wrote:

And yet when people try to educate you beyond your strawman understanding of said theory, and correct your arguments time after time, you seem to be unwilling to accept that you were wrong.

I have seen much of the same behavior amongst young earth creationists.

First of all, I’m Catholic; so let’s dispense with the YEC strawman approach to arguing.

Secondly, in this very post I’ve indicated serious problems with the interpretation of this experiment–some have admitted they were wrong; so why don’t you try a convincing argument, and then I’ll be happy to say I was wrong. No one has proved me wrong. There have only been allegations that I’m wrong. Big difference.

Thirdly, there have been plenty of noted biologists who have disagreed with Darwinian theory. Is that going to always be the “answer” to their protests? That is, “you simply don’t understand the theory.” Quite convenient–bordering on the fascist.

PvM wrote:

Sigh… So many problems first of all the density is now at 1/1000th the original density. If they are hard to detect at the full density why do you believe that at much lower densities they should be more visible.

Who said they were hard to detect at full density? If it’s a 1:4 ratio, AS I’VE STATED ALREADY, if you take a cell sample of 300-500 cells, that means you’ll see 75-125 empty mother cell walls. What’s so hard about that.

What makes me think that they can be seen at much lower densities? Fig 1a. Taken after 240 days (low unicell density), we clearly see an Ochromonus!!! It’s feeding on those LOW-DENSITY unicells!! It’s density is obviously LOWER than the unicells–but there it is!! Anymore questions you’d like to ask?

PvM wrote:

So far your argument seems mostly to be one of irrelevance. Does this mean that you have given up on your other irrefutable evidences? Look you have presented no evidence that these mother cells are ‘gone’, they are just present at much much lower concentrations.

You’re right. I haven’t presented any evidence that they’re gone. The AUTHORS DID!!!

p. 159 “The most probable initial mechanism for colony formation, adhesion of the duaghter cells ot the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation).”

And, Pim, who has refuted me? You say, “Well, you can’t see the mutant variant before the predation.” Why not? If that is what is being proposed, then why not take this Chlorella culture that has been cultured for 20 years, and go looking for the mutant? Are you trying to tell me that it’s there but you can’t find it? What are we dealing with? “Dark” mutant variants? (a la “dark matter” and “dark energy”)

So far, that has been YOUR ARGUMENT for Darwinism: the “mutant variant” is too dilute to be seen; the “mother cell walls” are too dilute to be seen. Is that really an argument? Isn’t that an argument from ignorance? Aren’t you simply pleading ignorance? Does this somehow ‘refute’ me?

PvM wrote:

Of course, this argument does not help you, in either instance there are these unicells which divide and motherwalls should be formed.

p. 160: “Colony growth was a ‘budding’ process, based on visual observations. Individual cells of the colony grew in size while dividing into daughter cells….” Then there’s Fig 1f. The AUTHORS say they can’t SEE cast off mother cell walls; and they tell us that they SEE a ‘budding process’. Along with Fig 1f., is it possible that the unicells, themselves, are ‘budding’, and not going through the mother cell mode of reproduction? I don’t know. But, again, it’s the AUTHORS who tell us that there are no ‘empty mother cell walls’. Why didn’t they bother giving us an explanation?

But your assumption about how many mother walls should be found needs to establish how many mother walls are to be expected and then you have to show that under your scenario this is better explained.

I disagree. It’s the author’s responsibility to do that. And it’s there responsibility to present data that supports their position.

PvM wrote:

Geez Blast, do the math.

If I had access to all the data and all the observations, then maybe I would be in a position to “do the math.”

Comment #86730

Posted by PvM on March 16, 2006 12:53 AM (e)

Blast wrote:

The problem with the theory is—since it seems impossible for any of you to understand plain English—it doesn’t add up. It’s highly improbable—like winning the lottery every week for 100 years; that improbable.

Totally unfounded assertion

Blast wrote:

No one has proved me wrong. There have only been allegations that I’m wrong. Big difference.

Till the end denying the obvious. Come on Blast… How dogmatic can one be.

Blast wrote:

Thirdly, there have been plenty of noted biologists who have disagreed with Darwinian theory. Is that going to always be the “answer” to their protests? That is, “you simply don’t understand the theory.” Quite convenient—bordering on the fascist.

Blast wrote:

But, again, it’s the AUTHORS who tell us that there are no ‘empty mother cell walls’. Why didn’t they bother giving us an explanation?

They did not say that there are no empty mother cell walls. They said they were virtually gone. When most cells are multicellular, the absence of mother walls shows that these cells do no lose the mother cell walls anymore. Read the discussion if you want to understand the authors’ explanation.

Blast wrote:

If I had access to all the data and all the observations, then maybe I would be in a position to “do the math.”

Why should we believe that you would do better with more data when you have done so poorly with the data presented so far? Look Blast, you are blaming many for your failures.

And yet you claimed ‘irrefutable’… In other words, is it not time to admit that you were wrong and that you lacked the data to show irrefutably that the authors were wrong?

Or is that too hard?

How often do you want to be shown to be wrong? And deny it…

Unsupported assertion, ad hominem and strawman. Not bad for a day’s job eh Blast. And the answer is no, the ‘you do not understand the theory’ is evidenced by your exhibited lack of understanding.

Blast wrote:

Who said they were hard to detect at full density? If it’s a 1:4 ratio, AS I’VE STATED ALREADY, if you take a cell sample of 300-500 cells, that means you’ll see 75-125 empty mother cell walls. What’s so hard about that.

Wrong again. Most of the cells are now multicellular. Only a very small fraction is single cellular and thus the lack of visible mother walls is not surprising.

Blast wrote:

What makes me think that they can be seen at much lower densities? Fig 1a. Taken after 240 days (low unicell density), we clearly see an Ochromonus!!! It’s feeding on those LOW-DENSITY unicells!! It’s density is obviously LOWER than the unicells—but there it is!! Anymore questions you’d like to ask?

The authors looked for some sample pictures and found an Ochromonus and one single cellular chlorella and one multicellular. Based on this you conclude what?

Blast wrote:

And, Pim, who has refuted me? You say, “Well, you can’t see the mutant variant before the predation.” Why not? If that is what is being proposed, then why not take this Chlorella culture that has been cultured for 20 years, and go looking for the mutant? Are you trying to tell me that it’s there but you can’t find it? What are we dealing with? “Dark” mutant variants? (a la “dark matter” and “dark energy”)

Yawn… lost for an argument Blast? And many have refuted your arguments which is why you are constantly moving the goalposts. Mutants were occasionally observed as expected. So what’s your problem. Your ‘irrefutable’ arguments have been mostly shown erroneous and you have yet to address the data in favor of the mutation theory.

Blast wrote:

So far, that has been YOUR ARGUMENT for Darwinism: the “mutant variant” is too dilute to be seen; the “mother cell walls” are too dilute to be seen. Is that really an argument? Isn’t that an argument from ignorance? Aren’t you simply pleading ignorance? Does this somehow ‘refute’ me?

Yes… It follows from the numbers Blast. Mother cells are virtually gone, as are the single cellular chlorella especially compared to the multicellular forms. It’s simple math.

Comment #86731

Posted by BlastfromthePast on March 16, 2006 12:55 AM (e)

PvM wrote:

Look Blast, if you do not care to educate yourself about evolutionary theory then why should we take your strawmen seriously?

Strawmen arguments, eh?

This is an abstract from the paper you suggested.

“The presence of the grazer Daphnia magna promoted formation of large colonies in the polymorphic green alga Scenedesmus subspicatus, but not so in the cyanobacterium Microcystis aeruginosa. For Scenedesmus this implies a change in the mode of reproduction, so that unicellular ‘Chodatella’ stages are induced to form eight-cell coenobial types. The same effect was observed on Scenedesmus whether adding live Daphnia or 1 ml of filtered water (0.45 microm) from an algal culture with daphnia present. After one day, the share of colonies increased in the treated cultures, and within 3-5 days, the majority of the cells were in 8-cell colonies heavily armored with spines. This increased cell dimensions from 6-8 x 4-5 microm in the unicells up to nearly 40 x 6 microm in the 8-cell colonies. These morphological changes seem induced by releases or biochemical substances from the grazer and could promote grazing resistance.”

Eight-celled colonies….how interesting. And it was ‘chemically induced’. Why is suggesting ‘chemical induction’ a ‘strawman’ argument?

PvM wrote:

I’d love to hear your argument especially since the data that explain the flaws in your argument are quite simple to find.

It’s not an argument; it’s a quote.

PvM wrote:

Hope this helps

Read Michael Denton’s criticism in “Evolution: A Theory in Crisis”. Hope that helps.

Darwin called ‘varieties’, ‘incipient species’. He was wrong. Very simple.

Comment #86732

Posted by PvM on March 16, 2006 12:55 AM (e)

Blast wrote:

p. 159 “The most probable initial mechanism for colony formation, adhesion of the duaghter cells ot the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation).”

Well there you have it. Large concentrations of multicellular chlorella means few predators and few single cellular and even fewer mother cell walls.

You asked “where are the mother cell walls’, logic and math shows that they are exactly where they are to be expected, surrounding the multicellular chlorella.

QED

Comment #86742

Posted by BlastfromthePast on March 16, 2006 1:19 AM (e)

PvM wrote:

Wrong again. Most of the cells are now multicellular.

I’m afraid it is you who are wrong, Pim. You failed to distinguish between the initial density and the lowered density.

PvM wrote:

They did not say that there are no empty mother cell walls. They said they were virtually gone.

They used the word “absence”. Please cite where they say that the mother cell walls were ‘virtually’ gone.

PvM wrote:

Based on this you conclude what?

I conclude what the authors themselves say: no mother cell walls were present; else you would see them.

PvM wrote:

Yawn… lost for an argument Blast?

Not at all. I’ve given one. Now refute it. I’m still waiting for a counter-argument to chemical induction that is persuasive and not just simple hand-waving.

PvM wrote:

Yes… It follows from the numbers Blast. Mother cells are virtually gone, as are the single cellular chlorella especially compared to the multicellular forms. It’s simple math.

This is what you wrote just a few paragraphs up: “The authors looked for some sample pictures and found an Ochromonus and one single cellular chlorella and one multicellular.” In one photograph you have BOTH this “low density” Chlorella, and this “low density” Ochromonus. Now how “dilute” are these “mutant variants”. You’re trying to tell me that you can’t find it if you look for it? If it’s as dilute as you imply it is, then it couldn’t possibly give rise to the 8-celled colonies that ‘appear’ after 10 days post inocculation. Math works both ways.

Comment #86744

Posted by BlastfromthePast on March 16, 2006 1:27 AM (e)

PvM wrote:

You asked “where are the mother cell walls’, logic and math shows that they are exactly where they are to be expected, surrounding the multicellular chlorella.

QED

And did you read my post where I used this very fact to suggest that ‘chemical induction’ is the best explanation for the ‘stickiness’ of the mother cell wall? Were you four-square behind then?

Comment #86748

Posted by BlastfromthePast on March 16, 2006 1:41 AM (e)

BLastfromthePast wrote:

Correct me if I’m wrong, but I think the proper formula would be something like (A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G, where A = the amount of Chlorella at t=0, w = the rate at which pefectly fit Chlorella are ‘washed out’ (go flying over the edge of the chemostat), w’ is the amount of A washed out at t=0, g = the number of Chlorella that are being ‘eaten’/hour (grazed) by the Ochromonus, g’ the amount of A grazed at t=0 and G is some ‘constant’ growth rate. (And, yes, A-w’-g’ can become a new constant A’—just as long as we take note of what “A’” is.) Taking the natural log of both sides yields: ln (A-g’-w’)x k*t - ln (g*t + w*t) = ln G

From this we can get:

ln (A-g’-w’)xk*t - ln [t(g+w)] = ln G

ln (A-g’-w’)k*t/ln [t(g+w)] = ln G

ln [(A-g’-w’)kt/t(g+w)] = ln G

Raising this equation by the power of “e”, we get:

(A-g’-w’)kt/t(g+w) = G

The “t”’s cancel on the left side. So,

G = (A-g’-w’)k/(g+w)

A, g’, and w’are all constants. k, g, and w are all assumed to be ‘constant’ rates. Hence,

G = Constant = growth rate. The ‘time’ has dropped out of this equation, so there’s no longer an exp(t) term anymore. It’s no longer time-dependent

This is probably better:

(A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G = r*t; where ‘r’ = ‘reproduction rate’.

Let A’= A-w’-g’ = constant; then,

Ln[A’ (exp)k*t] = ln [G + w*t + g*t]

Ln A’*k*t = ln [r*t + w*t + g*t]
Ln A’ x k*t = ln t x ln [r+w+t]

ln A’k x ln t = ln t x ln [r+w+t]

Dividing both sides by ln t, and taking the exponent of both sides:

A’k = r + w +g; solving for ‘r’:

r = A’k - w - g

A’ is a constant; k, w and g are all ‘rates’. Hence, ‘r’ (units wise) is also a ‘rate.’ (And absent the ‘exponential’, as Anton now agrees is correct.)

Anton also correctly interpreted who the ‘mathematician’ was.

Comment #86754

Posted by BlastfromthePast on March 16, 2006 2:18 AM (e)

W. Kevin wrote:

Um, check your math. If the initial density is 2 x 10^6 cells/ml, then the steady-state density of unicell Chlorella should be 2 x 10^3 cells/ml. Given that the empty cell walls should be at a 1:4 ratio, this equals a density of 5 x 10^2 walls/ml. At the sample sizes implied earlier (300-500 cells at a density of 2 x 10^6 cells/ml), that’s less than one cell wall per sample!

Are you by chance forgetting that the empty cell walls will be washed out of the chemostat?

Yes, in my haste, I forgot to divide by a thousand. It should be 5 x 10^2 wall/ml. Abstaining from power notation, there’s 500 mother cell walls/ ml., and at O.1 % of initial, 2000 cells/ml. That’s a 1:4 ratio. If you can find a Chlorella unicell, then if you take 4 samples, you can find 1 mother cell wall.

As far as the chemostat and washing out: again, think about it: if the authors thought that that was the cause of their ‘disappearance’, they would have told us so.

W. Kevin wrote:

Your prediction of sticky cell walls could have been cribbed directly from the paper (rhetorically speaking - I’m not accusing you of plagiarism, blast).

Or, you could have just looked at the photographs, too. It was pretty obvious what was going on. Fits my theory best.

W. Kevin wrote:

Where did the mother cell walls go? They remain as part of the colony. Your prediction wrt the “stickiness” of the mother cell walls is exactly the same as the evolutionary prediction, except with a different cause. Again, I fail to see how the data withheld on empty mother cell walls would support your hypothesis and simultaneously discredit the evolutionary hypothesis. Both require the same data (again, wrt empty cell walls). Do you understand yet?

Isn’t your last sentence a bit arrogant?

Re: “Where did the mother cell walls go? They remain as part of the colony. Your prediction wrt the “stickiness” of the mother cell walls is exactly the same as the evolutionary prediction, except with a different cause.”

How in the world can you say that ‘sticky’ cell walls is what ‘evolution [would] predict’? Evolution predicts NOTHING here. Tell me, what exactly in evolutionary theory ‘predicts’ that single cell phytoplankton, in the presence of a predator, will become ‘colonial’? I wasn’t ‘predicting’ cell wall ‘stickiness’ either. Chemical induction in this kind of experiment is what an ID perspective would predict; but it wouldn’t ‘predict’ the ‘colonial’ form. That just happens to be the case here.

You ask why the ‘cell wall data’ is necessary. Well, ‘cell walls’ aren’t living things in and of themselves; the unicells, and the colonies are. So, if what we see here is entirely a ‘cell wall’ phenomena, then you cannot posit a ‘mutant variant’–since ‘cell walls’ can’t duplicate.

Comment #86833

Posted by PvM on March 16, 2006 10:15 AM (e)

Blast wrote:

Strawmen arguments, eh?
This is an abstract from the paper you suggested….snip

Eight-celled colonies….how interesting. And it was ‘chemically induced’. Why is suggesting ‘chemical induction’ a ‘strawman’ argument?

I was not talking about chemical induction perse but rather your portrayal of evolution in general. Boraas considered induction and rejected it based on the evidence.

Blast wrote:

Read Michael Denton’s criticism in “Evolution: A Theory in Crisis”. Hope that helps.

Darwin called ‘varieties’, ‘incipient species’. He was wrong. Very simple.

I am sorry that you have a hard time making your own arguments. In addition, youhave yet to explain why Darwin was wrong.

Blast wrote:

PvM wrote:

Wrong again. Most of the cells are now multicellular.

I’m afraid it is you who are wrong, Pim. You failed to distinguish between the initial density and the lowered density.

Initially most cells are unicellular, however most of the unicellular cells are in the end ‘displaced’ by multicellular. You are wrong

Blast wrote:

They used the word “absence”. Please cite where they say that the mother cell walls were ‘virtually’ gone.

Hmm, I assumed you had read the paper

The cells in these stable colonies of predated cultures were enclosed within an envelope (Fig. 1d), apparently the mother cell wall of the neonatal cells (see Discussion). Empty mother cell walls were virtually absent from the culture.

Blast wrote:

Not at all. I’ve given one. Now refute it. I’m still waiting for a counter-argument to chemical induction that is persuasive and not just simple hand-waving.

Hmm, I assumed you had read the paper. You can lead a horse to water but you cannot make him drink. Read the discussion part.

Blast wrote:

You’re trying to tell me that you can’t find it if you look for it? If it’s as dilute as you imply it is, then it couldn’t possibly give rise to the 8-celled colonies that ‘appear’ after 10 days post inocculation. Math works both ways.

I have shown how your argument is wrong based on simple math Blast.

Blast wrote:

And did you read my post where I used this very fact to suggest that ‘chemical induction’ is the best explanation for the ‘stickiness’ of the mother cell wall? Were you four-square behind then?

And you are wrong based on logic and evidence. The mother cell walls cover the 8 cells or larger multicells… Have you read the paper?

Blast wrote:

As far as the chemostat and washing out: again, think about it: if the authors thought that that was the cause of their ‘disappearance’, they would have told us so.

Sigh, maybe authors work under the assumption that those reading their papers have some knowledge and understanding of chemostats.

Blast wrote:

You ask why the ‘cell wall data’ is necessary. Well, ‘cell walls’ aren’t living things in and of themselves; the unicells, and the colonies are. So, if what we see here is entirely a ‘cell wall’ phenomena, then you cannot posit a ‘mutant variant’—since ‘cell walls’ can’t duplicate.

Huh? Perhaps you can walk us through your cell wall argument again. Initially cell walls are present at high concentration since single cellular chlorella are present at high concentration. After the experiment most mother cell walls are gone which means that the prevalent 8 cellular forms arose without shedding of the mother cell wall. Photographic evidence and observation shows how the cell wall now covers the 8 cells.

What’s so hard to understand? Where did the mother cell walls go? They are now surrounding the 8 cells rather than being shed. If your question is where did the original mother cell walls go then the answer is simple, they washed out. That’s the whole idea behind a chemostat after all.

What happened to that irrefutable proof again Blast? Bit by bit it has been shown to be erroneous based on poor math or logic. What more can I say?

Comment #86838

Posted by David Wilson on March 16, 2006 10:39 AM (e)

In comment #86612:

Anton Mates wrote:

David Wilson wrote:

BlastfromthePast wrote:

As a mathematician, I don’t see how you can think Darwinism works.

….
In his application of the logarithm to obtain the left side of the last equation Mr Blast has committed at least two elementary blunders which anyone with a sound grasp of high-school mathematics (let alone someone claiming to be a “mathematician”) never should have.

In his defense, when Blast said “As a mathematician…”, I believe he was referring to me, not him.

In comment #86748:

BlastfromthePast wrote:

Anton also correctly interpreted who the ‘mathematician’ was.

In that case my misinterpretation of the comment has misled me into making my criticism harsher than was justified and I apologise for that.

BlastfromthePast wrote:

This is probably better: …

No, it’s still gibberish, and still contains several mistakes in the application of logarithms.

(A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G = r*t; where ‘r’ = ‘reproduction rate’.

Let A’= A-w’-g’ = constant; then,

Ln[A’ (exp)k*t] = ln [G + w*t + g*t]

Ln A’*k*t = ln [r*t + w*t + g*t]

No, the last equation doesn’t follow from any of the preceding calculations. Ln[A’* exp(k*t)] is not equal to Ln A’*k*t for any values of A’, k or t. The identity you are possibly groping for is Ln[A’* exp(k*t)] = Ln[A’] + k*t, but that doesn’t really help much in solving your original equation.

Ln A’ x k*t = ln t x ln [r+w+t]

ln A’k x ln t = ln t x ln [r+w+t]

And neither of these equation follows from any of the preceding calculations either. In general, ln(a * b ) is not equal to ln(a) x ln(b), but ln(a) + ln(b).

Comment #86856

Posted by BlastfromthePast on March 16, 2006 12:55 PM (e)

This is probably better:

(A-w’-g’)exp(k*t)- w*t - g*t = constant= growth rate =dilution rate = G = r*t; where ‘r’ = ‘reproduction rate’.

Let A’= A-w’-g’ = constant; then,

Ln[A’ (exp)k*t] = ln [G + w*t + g*t]

Ln A’*k*t = ln [r*t + w*t + g*t]
Ln A’ x k*t = ln t x ln [r+w+t]

ln A’k x ln t = ln t x ln [r+w+t]

Dividing both sides by ln t, and taking the exponent of both sides:

A’k = r + w +g; solving for ‘r’:

r = A’k - w - g

A’ is a constant; k, w and g are all ‘rates’. Hence, ‘r’ (units wise) is also a ‘rate.’ (And absent the ‘exponential’, as Anton now agrees is correct.)

Here’s how it should go:

G = (A - wt - gt)(exp)k*t [1]

G is constant.

We have “steady-state” conditions; therefore:

dG/dt = 0 [2]

dG/dt = [(A -wt -gt)k(exp)k*t] + [(-w-g)(exp)k*t = 0 [3]

We divide the equation by (exp)k*t, and:

(A -wt -gt)k = (w + g) [4]

k = (w + g)/ (A -wt -gt) [5]

A, w, and g are all constant; hence

k = constant/time = constant growth rate.

QED

Comment #87014

Posted by W. Kevin Vicklund on March 16, 2006 10:04 PM (e)

k = (w + g)/ (A -wt -gt) [5]

A, w, and g are all constant; hence

k = constant/time = constant growth rate.

QED

Well, it seems blast has finally figured out how to properly manipulate logarithms. Unfortunately, his final analysis is incorrect - he just proved that his equation is not the correct one. Since we are in steady-state, k should be a constant (dk/dt=0), or time-invariant. The correct equation should produce an equation for k without any t. At t=0, k=(w+g)/A, but as t increases, the denominator decreases and k eventually goes to infinity at (w+g)t=A, and then as t approaches infinity, k approaches 0 from negative infinity.

BTW, I calculated the evaporation rate for a 500 mL chemostat. If the numbers I was given are roughly accurate, we should expect an evaporation rate of about 1 ml/hr. Obviously, since I don’t know the conditions of the lab, this number is quite rough (for example, high humidity would decrease the evaporation rate). However, it certainly looks as if the 0.035 ml/hr rate is using the wrong units and should be L/hr instead (or perhaps mL/s?).

Comment #87245

Posted by BlastfromthePast on March 17, 2006 1:14 PM (e)

Since we are in steady-state, k should be a constant (dk/dt=0), or time-invariant. The correct equation should produce an equation for k without any t. At t=0, k=(w+g)/A, but as t increases, the denominator decreases and k eventually goes to infinity at (w+g)t=A, and then as t approaches infinity, k approaches 0 from negative infinity.

You’re right, Kevin. Please feel free to come up with your own equation.

Comment #87263

Posted by Anton Mates on March 17, 2006 2:05 PM (e)

OK, so what quantities are we finding formulas for?

Since the objective here is (so far as I know) to determine generation times, it makes sense to look at B(t), the number of Chlorella cells (or colonies, whichever morph interests you) produced by time t. Consider also D(t), the number of cells which have been lost to death or washout between times 0 and t. So B(0) is your initial population size, D(0) = 0, and your population size at any time is B(t) - D(t). The generation time TG(t) is the time it takes for the population, starting at time t, to produce a number of cells equal to its own size (at time t):
B(t+TG)-B(t)= B(t)-D(t).
As indicated, TG(t) could vary with time (though fortunately it doesn’t for the cases considered.)

What quantities can be taken as constant? The dilution rate k, measured (say) as a fraction of total chemostat volume per unit time, and the maximum Chlorella growth rate K. Of course k ≤ K or else the Chlorella washes out completely.

What else is good to include; probably P(t), the number of Chlorella cells specifically lost to predation. P’(t) is at least roughly constant in a steady-state situation, but in general varies all over the place. Of course it’s never negative.

In a predatorless steady state, cells are lost only by medium dilution, so the rate of loss is the product of the dilution rate and the current population size: D’(t)=k*(B(t)-D(t)). By assumption of steady state,
D’(t)=B’(t)
so that the population’s rate of change (B’(t)-D’(t)) is zero and the pop. size remains at B(0) for all time. Thus
B’(t)=k*B(0)
B(t) = k*B(0)*[t+1]
Then TG, the generation time, is simply 1/k, as shown by the following:
B(t+TG)-B(t)=k*B(0)*[(t+TG+1) - (t+1)]=B(0)
k*TG=1.

In a predator-present well-grazed steady state, cells are lost by medium dilution at the previous fractional rate, but also to predation:
D’(t)=k*(B(t)-D(t))-P’. (Assume P’ is constant since it’s a steady state.) Again, the population is always B(0), and B’(t)=D’(t). So
B(t)=k*B(0)[t+1]+P’*t. Then
TG = 1/[k + P’/B(0)].

Note that, as Kevin said, TG is smaller now. In fact, it’s probably equal to 1/K; the severely-reduced Chlorella population no longer has overcrowding and nutrient competition slowing down its growth, and will therefore grow at its maximum rate K. (This requires “fine tuning” of the predation rate so that P’ = (K-k)*B(0), but that should occur automatically by assumption of steady state. If the predation rate is slower or faster, the populations will adjust to correct it.)

In an exponentially-growing transient state, as occurs at the start of the culture or after each population crash, the predation rate (if there’s predators at all) is small enough to be neglible compared to the loss from medium dilution, and the Chlorella will grow at its maximum rate K. Therefore
B’(t)=K*[B(t)-D(t)] and
D’(t)=k*[B(t)-D(t)];
the total population size is B(0)*exp([K-k]*t), so
B(t)=B(0)*[K*exp([K-k]*t)-k]/[K-k]. Then TG is ln(2-[k/K])/[K-k].

In a state of exponential population crash, the generation time is virtually infinite, simply because the total number of Chlorella that will ever be produced converges to a finite number. Or, more realistically, the population will stop crashing and start doing something else before a generation’s elapsed.

So, to summarize and plug in the (corrected) dilution rate and Chlorella’s max growth rate as estimated by Kevin: Generation times will be about 14 hours for unicells in steady state without predators, about 9 hours for unicells in steady state with predators, about 8 hours for unicells whose population is recovering exponentially, and effectively infinite for unicells experiencing population crashes.

Of course none of these are valid over the long term when you’ve got predator-prey oscillations and whatnot, as just before the colonial morphs appear; to calculate that you’d need much more info than we have (such as the Ochromonas predation success rate as a function of the densities of the various organisms) in order to solve the interdependent differential equations describing the various populations over time.

Comment #87311

Posted by W. Kevin Vicklund on March 17, 2006 4:28 PM (e)

For the sake of completeness, we should also note the growth rate of colonies and predators in steady-state is the flow rate, or a generation time of 14 hours for each in steady-state. This is assuming the unicell population is also at steady-state and not fluctuating, of course.

Comment #87623

Posted by David Wilson on March 18, 2006 9:59 AM (e)

In comment #87245

BlastfromthePast wrote:

Since we are in steady-state, k should be a constant (dk/dt=0), or time-invariant. The correct equation should produce an equation for k without any t. At t=0, k=(w+g)/A, but as t increases, the denominator decreases and k eventually goes to infinity at (w+g)t=A, and then as t approaches infinity, k approaches 0 from negative infinity.

You’re right, Kevin. Please feel free to come up with your own equation.

As Kevin has already pointed out, the changes in the concentrations of the organisms and nutrients in the chemostat are governed by a system of differential equations. Here is another simple model for just a single predator and a single prey:

dμ/dt = g1( μ, ν, ζ ) μ - f μ/V

dν/dt = g2( μ, ν ) ν - f ν/V .

dζ/dt = g3( μ, ζ ) μ + f c/V - f ζ/V

Here, μ and ν are the densities of the prey and predator, respectively, in numbers of organisms per litre (say) in the chemostat, ζ is the density of nutrient in grammes per litre in the chemostat, c is its density in grammes per litre in the inflow, f is the flow rate in litres/hour (say) and V is the volume of the contents of the chemostat in litres.

g1( μ, ν, ζ ) and g2( μ, ν ) are what the hourly growth rates of the prey and predator would be at the densities μ, ν, ζ of the various ingredients of the chemostat in the absence of any dilution by the inflow or losses to the outflow.

g3( μ, ζ ) is the number of grammes per hour of nutrient that a single prey organism consumes at the densites μ, ζ of the organism and nutrient.

Unless the contents of the chemostat have reached a steady state, μ, ν and ζ would all be functions of time. All the remaining quantities, c, f and V, can be assumed to be constant.

The possible steady-state concentrations of the ingredients of the chemostat can be obtained by finding the values of them that would maintain their time derivates constantly at 0—i.e. by solving the following system of equations for the quantities μe, νe and ζe:

0 = g1( μe, νe, ζe ) μe - f μe/V        (1)

0 = g2( μe, νe ) νe - f νe/V        (2)

0 = g3( μe, ζe ) μe + f c/V - f ζe/V        (3)

As a very simple (or perhaps “simplistic” would be a better word) first approximation we could take g1 amd g2 to have something like the following forms:

g1( μ, ν ) = k1 (1 - μ/μmax) - w ν

g2( μ ) = k2 (μ - μmin)

In this simplified model k1 (1 - μ/μmax) is the natural hourly growth rate of the prey in the absence of the predator (ν = 0) and any inflow to or outflow from the chemostat. This gives a simple logistic model for the growth of the prey population.

w μ is the number of prey organisms consumed per hour by a single predator. In the simplified model it is assumed to be simply proportional to the concentration of prey (i.e. w is assumed constant). While this is an extremely crude assumption, it’s probably not too unreasonable for very small concentrations of the prey.

k2 (μ - μmin) is the natural hourly growth rate of the predator at the given concentration μ of the prey. The simplified model makes another extremely crude assumption that this is simply an affine function of the prey concentration.    μmin is the minimum concentration of prey sufficient to prevent the population of predators from declining. When μ > μmin, and in the absence of losses to the outflow from the chemostat, it is assumed that the number of predators would grow exponentially at the rate k2 (μ - μmin). Likewise, when μ < μmin, it is assumed that the number of predators would decline exponentially at that rate (negative, in this case).

In the absence of any inflow and outflow from the chemostat this simplified model reduces to a slightly generalised version of the Lotka-Volterra model for predator-prey interactions.

With these simple forms for g1 and g2, equations (1) and (2) above have exactly three steady-state solutions when f/V < k1 (but only one if f/V > k1).

In the first case the steady-state solutions are:

μe = νe = 0,

μe = μmax, νe = 0,  and

μe = μmin + f/(k2V),  νe = ( k1 ( 1 - μemax) - f/V )/w;.

In the third of these, the natural growth rates of the prey and predator are constant at w νe + f/V, and f/V, respectively—exactly sufficient to balance the losses due to consumption of the prey by the predator and the outflow from the chemostat.

Comment #87633

Posted by 'Rev Dr' Lenny Flank on March 18, 2006 11:13 AM (e)

Read Michael Denton’s criticism in “Evolution: A Theory in Crisis”. Hope that helps.

Then read (1) Denton’s next book, which explains why his previous book was wrong, and (2) Denton’s request to be removed from the DI’s list of Fellows and supporters.

Hope that helps.

Comment #87649

Posted by PvM on March 18, 2006 5:25 PM (e)

I’d like to hear Blast explain why Darwin was wrong about varieties and incipient species? And why should we rely on Denton whose book seems in many aspects to be quite flawed.

Comment #88023

Posted by BlastfromthePast on March 20, 2006 8:52 PM (e)

I’ve allowed myself, let us say, a ‘cooling off period.’

I’m very disillusioned with the attitude of the people on this board—and that includes you, Pim.

You all seem to lack any ability whatsoever to admit that there might be problems should those problems tend to undermine, in any way at all, the hallowed Darwinian orthodoxy.

PvM wrote:

Hmm, I assumed you had read the paper
“The cells in these stable colonies of predated cultures were enclosed within an envelope (Fig. 1d), apparently the mother cell wall of the neonatal cells (see Discussion). Empty mother cell walls were virtually absent from the culture.”

Yes, I’ve read the paper more than once. And I also read, “The most probable initial mechanism for colony formation, adhesion of the daughter cells to the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies (Fig. 1d) and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation).” So, which is it? Are they ‘virtually absent’, or are they ‘absent’, period? Wouldn’t it be nice to know?

This points out a serious problem with this paper: inconsistency in reporting and terminology. Where were the peer-reviewers?

As I say, it’s a serious problem.

We’ve already gone round and round on this: but what, exactly, constitutes a “multicell”? On one page of their paper they call it a ‘colony’, then it’s a ‘multicell colony’, and then they talk flat out about ‘multicells’. Why can’t they get their terminology consistent? Again, where are the peer-reviewers?

They’re also inconsistent in their reasoning.

For example, what is their reason for ‘discounting’ chemical induction? The principal reason given is that: “First, colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates. An ‘induction’ should have been expressed as soon as the inducing substance produced by the flagellates had reached some critical concentration.” (p. 159) Yet, on the SAME PAGE, they write: “In a system where environmental conditions were held constant, a multicellular organic form evolved from a unicellular one within 10±20 generations.” Well, again, which IS IT: 10 or 20 generations? When it comes to their MAIN reason for discounting chemical induction, they equivocate! Amazing!

So, how many generations are we talking about? Well, on page 155 they write: “This reduction in predation pressure allowed the Chlorella population to recover and increase rapidly, …During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days).”

So the unicells are grazed down for the first five days, and then in the next five days, ‘colonies’ appear. To get 20 generations into 5 days requires a growth rate of 6 hours. We know that’s wrong.

“Oh, but it’s not 5 days, it’s 10 days.” you say, since the Ochromonus was ‘introduced’ on the first day.

Well, then, what meaning shall we give to their acknowledgement that a “critical concentration” of the flagellates must be reached? Do the authors help us out? Of course not! But we’ve come to expect that by now.

Shall we assume the ‘critical concentration’ was reached in the first hours after inoculation? That seems completely unsupportable, but from their conclusions, that appears exactly what they reasoned. So here we have an issue that the authors bring up–the ‘critical concentration’ of an inducer–, but they do so without giving any explanation for it, and without demonstrating any effort on their part to determine if, indeed, such a concentration occurred, or when. We’re left dangling—as in almost everything in this paper.

Now, when did this possible ‘triggering’ occur. Well, if they want to ‘discount’ the possibility of chemical induction, then, as scientists, they should take the most conservative estimate possible of when, exactly, the ‘chemical trigger’ occurred. The most conservative estimate would be 7 days after inoculation (in papers on chemical induction in Scenedesmus, they say the response begins after 48 hours of introduction of the chemical inducer.) But certainly, after 5 days, at a time when the unicell density is very low and the Ochromonus is high, one can certainly say the ‘trigger’ has been signaled. So, that’s fairly conservative. Now, taking that conservative ‘time’ for the ‘trigger’, that leaves 5 days for the colonial forms to multiply and become evident. Well, how many generations does that represent? Do the authors help us? No, not really. But, after much difficulty, those posting here have come up with a number for the growth rate that is equal to the dilution rate. That number is 14.6 hours. But that 14.6 hours includes ‘wash out’ of some cells. The fastest time given on this post was around 10 hours (from memory: 9.9 hrs).

But there’s another factor to take into account. Boxhorn, one of the authors, writes on Talk.Origins.com, that the growth rate of strains that are competing for nutrient in a chemostat can be skewed depending on which form is dominating. And on page 158, in the legend, they write: “The majority of Chlorella cells were in colonies with more than 24 cells per colony for the first month of culture. The large colonies then disappeared from the culture and the number of cells per colony stabilized at eight.”

So, they first say that ‘colonies’ did not become apparent for about 20 Chlorella generations. But if the ‘multicells’ are dominant for the first month, then that means the growth rate of the ‘colonies’ will be less (perhaps much less) than that of the ‘multicells’. And since to ‘conservatively’ rule out chemical induction we’ve taken the 5-day mark as the time of the ‘trigger’; and since the authors tell us that on day 10 the ‘colonial’ forms were seen, that means that to determine the number of generations involved in the colonial forms appearance, we divide the 5 days by the growth rate. What growth rate should we take? I would say that it should be at least around the 14.6 hr/ generation mark. But to be ‘conservative’, let’s take 20 hrs. Then we’re looking at 6 generations—which is well within the range for chemical induction.

In one paper on chemical induction of Scenedesmus, the authors say that it takes 48 hours in the presence of the chemical inducer before anything happens, and that it takes 3-5 days (!!!) for the colonial forms to appear. So, in the paper at hand, if the ‘chemical inducer’ began to be produced after 3 days, then on the 5-day mark, the unicells would begin to react. And it would take them 3-5 days to appear. Translated, this means that by the 10 day mark the colonial forms would be expected to be present—which is, of course, exactly what the authors of the Boraas paper report. And why (if you deny that this was not an important fact to report, then you’re in complete denial) didn’t the authors tell us what was going-on on Day-8? Were the colonial forms already present? Why don’t they tell us, one way, or the other. This paper, in NO WAY, ‘discounts’ chemical induction.

I’m tiring of all of this. I could easily go on and point out that what we see is best explained as a ‘mother cell wall’ phenomena; and to point out that ‘multicellularity’ is never really achieved or arrived at [although it’s the authors main thesis. At best, the cells just simply ‘cling’ to the mother cell walls, which themselves cling to one another]. But as I say, I tire of all the nonsense on this board.

I’ll just leave you with this quote from a 2004 review article:
(Plant Physiology, January 2004, Vol. 134, pp. 1–2,)

“Colonies of Chlamydomonas and Chlorella spp. stimulated quorum sensing-dependent luminescence in Vibrio harveyi, indicating that these algae may produce compounds that affect the quorum sensing system in Vibrio species.”

And this quote from a 2003 review paper: (Phenotypic plasticity in the green algae Desmodesmus and Scenedesmus with special reference to the induction of defensive
morphology, M. Lürling; Ann. Limnol. - Int. J. Lim. 39 (2), 85-101)

“In fact, in culture unicells may be very common (e.g. Hegewald 1982, Holtmann & Hegewald 1986, Lürling & Beekman 1999, Trainor 1998), even at cell density far above ca. 1000 cells.ml-1. Hence, low cell density (Egan & Trainor 1989b) does not seem a prerequisite for unicell development in several Desmodesmus and Scenedesmus strains.

And why are there that few reports of unicellular Desmodesmus and Scenedesmus
from the field ? One explanation could be that due to the activity of grazers unicells are produced only in very low numbers, which experience a high mortality ; protective colonies are being induced. Trainor (1979) observed that unicells disappeared when incubated in dialysis sacks in the field or when cultured in pond water in the laboratory. Interestingly, in another study ten years later the same strain produced unicells in water from the same pond (Egan & Trainor 1989b,d). Perhaps the activity of grazers had been involved in this plasticity and grazer-associated chemical cues might account for the different observations by Trainor (1979) and Egan & Trainor (1989b,d). Also colonial D. abundans from the field formed unicells in the laboratory (Fott 1968). Another reason may be that unicells are simply not recognized as Scenedesmus. Opening a textbook one will find Desmodesmus and Scenedesmus presented as «a freshwater colonial green alga» often supported with images of four-celled coenobia. Unicells may resemble species described in at least eight other green algal genera (Trainor 1998). Kessler and co-workers using sequence analyses of 18S rDNA showed that two taxa of the unicellular Chlorella were in fact unicellular Scenedesmus while one Chlorella and one Kermatia had to be designated to Desmodesmus (Kessler et al. 1997)
!!!!

Adieu.

Comment #88026

Posted by BlastfromthePast on March 20, 2006 8:58 PM (e)

PvM wrote:

I’d like to hear Blast explain why Darwin was wrong about varieties and incipient species? And why should we rely on Denton whose book seems in many aspects to be quite flawed.

Because ‘chihuahuas’ aren’t about to form a ‘new species’ of Canus familiaris.

And, of course, Pim, that’s what all evolutionists say to criticism of their hallowed theory: it’s wrong; it’w flawed’ they don’t know anything about evolutionary theory, blah, blah, blah.

And Lenny, if you think that Denton contradicts himself in his “Nature’s Destiny”, I can only conclude–once again–that you’ve read neither one of them. You’re flat out wrong. Not every review you read on the internet–just because it appeals to you–happens to be factual.

Comment #88030

Posted by BlastfromthePast on March 20, 2006 9:02 PM (e)

Finally, the derivations of Anton and David Wilson both look fairly good.

I’ve looked at some papers on mixed species chemostats that deal with the mathematics, and they’re quite complicated. I think your equations, though simplified, are helpful. (Maybe I should say that BECAUSE they are simplified, they’re helpful–a compliment.)

Comment #88092

Posted by PvM on March 20, 2006 11:24 PM (e)

Blast wrote:

I’m very disillusioned with the attitude of the people on this board—and that includes you, Pim.

You all seem to lack any ability whatsoever to admit that there might be problems should those problems tend to undermine, in any way at all, the hallowed Darwinian orthodoxy.

Wow, that’s quite a jump from showing that your ‘irrefutable evidence’ hardly matched that description and was mostly based on a confusion as to what the authors actually argued.

So why are you creating this strawman argument?

In fact, even if you were right, I fail to see how this would undermine evolutionary theory?

Other than that Blast’s ‘response’ is not much different from earlier attempts, blaming others including the authors of the paper for his confusion and calling this a ‘serious problem’.

PvM wrote:

I’d like to hear Blast explain why Darwin was wrong about varieties and incipient species? And why should we rely on Denton whose book seems in many aspects to be quite flawed.

Because ‘chihuahuas’ aren’t about to form a ‘new species’ of Canus familiaris.

And, of course, Pim, that’s what all evolutionists say to criticism of their hallowed theory: it’s wrong; it’w flawed’ they don’t know anything about evolutionary theory, blah, blah, blah.

Another fascinating strawman. Just because many of your ‘criticisms’ were found to be ill conceived does not mean that any and all such criticism is flawed’.

Why not focus on your claim about Darwin.
How and why do you believe Darwin was wrong and how is your ‘example’ relevant? After all we do know of examples of speciation. Are you perhaps confusing Darwin’s explanation of how speciation happens with his ideas about speciation?

And Lenny, if you think that Denton contradicts himself in his “Nature’s Destiny”, I can only conclude—once again—that you’ve read neither one of them. You’re flat out wrong. Not every review you read on the internet—just because it appeals to you—happens to be factual.

ROTFL now that’s irony at work.

Btw it’s “canis familiaris”

Comment #88094

Posted by PvM on March 20, 2006 11:29 PM (e)

And note how Blast seems to ignore the other reasons given why the authors reject the induction hypothesis. Somehow Blast took one, called it the ‘principal reason’ and avoids dealing with the overall reasons presented.

Irrefutable indeed…

Comment #88111

Posted by Sir_Toejam on March 21, 2006 12:06 AM (e)

Pim-

you do of course, realize that your simply feeding his delusions by the simple act of responding to them, yes?

The one thing I’ll give Blast over Larry is that he rarely spreads himself to other threads once focused on a particular non-issue.

logic levels are about the same, tho.

Comment #88115

Posted by k.e. on March 21, 2006 12:19 AM (e)

Careful Blast you are only a few day away.
APRIL FOOL, n. The March fool with another month added to his folly.**

Why is it whenever the noose tightens you project ?
Evolutionist this…… evolutionist that.
Your absolute classic was DarwinistsCreationists have been denying creationismevolution for 150 years.

Why align yourself with such an intellectually vapid and sine nobilis bunch of cultural miscreants ?
A fringe group of knowledge pygmy’s ?
Uneducated cultural slobs who think religion IS culture. ?
Frightened that their hold on reality as described to them around 5 years old was just an elaborate fantasy.
Wasting their lives and those of others justifying the unjustifiable.

Your should start your own eduKational intuition Blast , you have no need of knowledge.

Comment #88204

Posted by BlastfromthePast on March 21, 2006 1:49 PM (e)

The fact that two ‘taxa’ of Chlorella have been shown to actually be Scenedesmus, which is known to form a 8-cell colonial form through chemical induction, doesn’t seem to slow you down one bit, does it? Just pretend I never pointed it out.

Good-bye, Panda’s Thumb.

Comment #88316

Posted by W. Kevin Vicklund on March 21, 2006 6:46 PM (e)

I don’t know if blast will ever read this, but I’ll post it anyways. Besides, other people may learn stuff.

I’ve allowed myself, let us say, a ‘cooling off period.’

I’m very disillusioned with the attitude of the people on this board—and that includes you, Pim.

You all seem to lack any ability whatsoever to admit that there might be problems should those problems tend to undermine, in any way at all, the hallowed Darwinian orthodoxy.

Our attitude might be more positive if you would show any propensity to argue in good faith. Instead, you continue to deliberately misconstrue the arguments made in the paper and by the people posting on this board.

PvM wrote:

Hmm, I assumed you had read the paper
“The cells in these stable colonies of predated cultures were enclosed within an envelope (Fig. 1d), apparently the mother cell wall of the neonatal cells (see Discussion). Empty mother cell walls were virtually absent from the culture.”

Yes, I’ve read the paper more than once. And I also read, “The most probable initial mechanism for colony formation, adhesion of the daughter cells to the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies (Fig. 1d) and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation).” So, which is it? Are they ‘virtually absent’, or are they ‘absent’, period? Wouldn’t it be nice to know?

First of all, since “virtually absent” is used first, it takes precedence. Secondly, the absence of mother cell walls is a “personal observation” which means the observation is not meant to be formal data. When you look at their methods, they were objectively determining the amount of cells of various sizes via the Celloscope, but not the number of empty mother cell walls. It appears that mother cell walls were only reliably detected with direct (microscopic) observation, which used smaller sample sizes than the Celloscope. Therefore, since the unicells were present at .1% of their initial levels, we would expect the cast-off walls to be present at a similarly reduced rate. Which means that instead of a visual field teeming with these empty cell walls, we would only rarely see a cell wall - they are virtually absent.

But I must confess, this particular argument of yours seems exceedingly pointless. For either of our models to be internally consistent, low but non-zero levels of empty cell walls (proportional to the unicell density) need to be present during the steady-state unicell-colony-predator chemostat.

This points out a serious problem with this paper: inconsistency in reporting and terminology. Where were the peer-reviewers?

As I say, it’s a serious problem.

The only problem is the artificial problems you are creating by deliberately misreading and misconstruing the paper.

We’ve already gone round and round on this: but what, exactly, constitutes a “multicell”? On one page of their paper they call it a ‘colony’, then it’s a ‘multicell colony’, and then they talk flat out about ‘multicells’. Why can’t they get their terminology consistent? Again, where are the peer-reviewers?

Their terminology is consistent - colonies and multicells are synonymous. You are trying to force a dichotomy that isn’t there. The failing is on your deliberate attempt to create problems that don’t exist on baseless assumptions.

They’re also inconsistent in their reasoning.

For example, what is their reason for ‘discounting’ chemical induction? The principal reason given is that: “First, colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates. An ‘induction’ should have been expressed as soon as the inducing substance produced by the flagellates had reached some critical concentration.” (p. 159) Yet, on the SAME PAGE, they write: “In a system where environmental conditions were held constant, a multicellular organic form evolved from a unicellular one within 10±20 generations.” Well, again, which IS IT: 10 or 20 generations? When it comes to their MAIN reason for discounting chemical induction, they equivocate! Amazing!

They give four reasons. They do not have to be in any particular order of preference. They make no claim to it being their main reason, just one of four. And the other three are devastating to your induction hypothesis - you are picking on what may be the weakest argument. But setting that aside, there is a difference between the time to appearance of colonies and the time to evolve. It was approximately 20 generations before the colonial form started appearing in their microscopic scans. That does not mean that it wasn’t present before then, just that it wasn’t present in densities large enough to be noticeable in small sample sizes. My own interpretation of their use of evolve is that selection for colonies didn’t begin until 10-20 generations, rather than a mutation event occurring somewhere during that time period (though I don’t rule that out).

So, how many generations are we talking about? Well, on page 155 they write: “This reduction in predation pressure allowed the Chlorella population to recover and increase rapidly, …During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days).”

So the unicells are grazed down for the first five days, and then in the next five days, ‘colonies’ appear. To get 20 generations into 5 days requires a growth rate of 6 hours. We know that’s wrong.

Actually, we don’t know that 20 generations into 5 days is wrong (and again, you have your units wrong - growth rate is in units of inverse time). We have repeatedly informed you that determining growth rate from flow rate only works during steady-state, non-predatory conditions. The growth rate will definitely increase during the first 8 days, at the very least. We haven’t determined the actual max growth rate of Chlorella, but what we have found through a literature search is that the minimum generation time is less than or equal to 8 hours. That gives us 6-7 days for 20 generations, but is not definitive.

“Oh, but it’s not 5 days, it’s 10 days.” you say, since the Ochromonus was ‘introduced’ on the first day.

Well, then, what meaning shall we give to their acknowledgement that a “critical concentration” of the flagellates must be reached? Do the authors help us out? Of course not! But we’ve come to expect that by now.

Shall we assume the ‘critical concentration’ was reached in the first hours after inoculation? That seems completely unsupportable, but from their conclusions, that appears exactly what they reasoned. So here we have an issue that the authors bring up—the ‘critical concentration’ of an inducer—, but they do so without giving any explanation for it, and without demonstrating any effort on their part to determine if, indeed, such a concentration occurred, or when. We’re left dangling—as in almost everything in this paper.

Simple examination of the data from Figure 2a shows that the Ochrimonus population had in fact peaked by Day 1. The data given supports the conclusion that a critical concentration was indeed present a few hours after inoculation - call it 12 hours, as that corresponds to twice the doubling time (given as 6 hours in the paper). The relative populations sizes don’t appear to be able to sustain an initial population boom of much more than that. The data is right there for us to see.

Now, when did this possible ‘triggering’ occur. Well, if they want to ‘discount’ the possibility of chemical induction, then, as scientists, they should take the most conservative estimate possible of when, exactly, the ‘chemical trigger’ occurred. The most conservative estimate would be 7 days after inoculation (in papers on chemical induction in Scenedesmus, they say the response begins after 48 hours of introduction of the chemical inducer.) But certainly, after 5 days, at a time when the unicell density is very low and the Ochromonus is high, one can certainly say the ‘trigger’ has been signaled. So, that’s fairly conservative. Now, taking that conservative ‘time’ for the ‘trigger’, that leaves 5 days for the colonial forms to multiply and become evident. Well, how many generations does that represent? Do the authors help us? No, not really. But, after much difficulty, those posting here have come up with a number for the growth rate that is equal to the dilution rate. That number is 14.6 hours. But that 14.6 hours includes ‘wash out’ of some cells. The fastest time given on this post was around 10 hours (from memory: 9.9 hrs).

First of all, Figure 2a clearly shows that Ochrimonus density is at a minimum at Day 5, not a maximum! Boraas et al even pointed this out. Perhaps you misread the paper yet again. The data is clear - if there was a critical concentration, it occurred within the first day. And where on earth are you getting “after 48 hours” from? Of the half dozen papers on colony inducement in Scenedesmus I was able to look at online, they all stated that within 48 hours colonies were the dominant form. Not just appearing, but dominant. BTW, the steady-state generation time (based solely on flow rate) is just under 14.3 hours (the growth rate is properly 0.07 h-1). But, as stated numerous times previously, the actual growth rate during these initial stages will be faster (the quickest generation time as posted here was estimated at about 8 hours, from other literature).

So the most conservative estimate based on real data would be 1 day (max concentration) + 2 days (time to dominate) = 3 days. We should see some sort of peak in Figure 2a sometime in Day 1-3, but we don’t.

But there’s another factor to take into account. Boxhorn, one of the authors, writes on Talk.Origins.com, that the growth rate of strains that are competing for nutrient in a chemostat can be skewed depending on which form is dominating. And on page 158, in the legend, they write: “The majority of Chlorella cells were in colonies with more than 24 cells per colony for the first month of culture. The large colonies then disappeared from the culture and the number of cells per colony stabilized at eight.”

So, they first say that ‘colonies’ did not become apparent for about 20 Chlorella generations. But if the ‘multicells’ are dominant for the first month, then that means the growth rate of the ‘colonies’ will be less (perhaps much less) than that of the ‘multicells’. And since to ‘conservatively’ rule out chemical induction we’ve taken the 5-day mark as the time of the ‘trigger’; and since the authors tell us that on day 10 the ‘colonial’ forms were seen, that means that to determine the number of generations involved in the colonial forms appearance, we divide the 5 days by the growth rate. What growth rate should we take? I would say that it should be at least around the 14.6 hr/ generation mark. But to be ‘conservative’, let’s take 20 hrs. Then we’re looking at 6 generations—which is well within the range for chemical induction.

Again, colonies and multi-cells are synonymous. But your analysis is completely wrong. This is a chemostat. In order to avoid “washing out” the growth rate must be at least equal to the dilution rate (as determined by the flow rate and the volume of the chemostat), regardless of what any other population is doing. In order for a population to grow, the growth rate must be faster than the dilution rate. The most conservative estimate, no growth, is 14.3 hours/generation, or a growth rate of 0.07 gen/hr. In reality, since the population is growing, we would be looking at something more like 12.5 hr/gen, or a growth rate of 0.08 gen/hr, as a conservative estimate - which is pretty close to an estimate of 20 generations in 10 days. 20 hr/gen is right out. Again, flow-rate is only definitive for steady-state, it is merely a boundary for transient states.

Larger colonies should have slower growth rates than smaller colonies, but it appears that the larger colonies start out with higher absolute numbers. Once we reach steady-state (in terms of unicell-colony-predator populations), the growth rate of smaller colonies will then be slightly faster than the dilution rate, and the growth rate of the larger colonies will then be slightly slower than the dilution rate. This leads to a slow washing out of the larger colonies and corresponding increase of smaller colonies, at a rate determined by the difference in growth rates.

In one paper on chemical induction of Scenedesmus, the authors say that it takes 48 hours in the presence of the chemical inducer before anything happens, and that it takes 3-5 days (!!!) for the colonial forms to appear. So, in the paper at hand, if the ‘chemical inducer’ began to be produced after 3 days, then on the 5-day mark, the unicells would begin to react. And it would take them 3-5 days to appear. Translated, this means that by the 10 day mark the colonial forms would be expected to be present—which is, of course, exactly what the authors of the Boraas paper report. And why (if you deny that this was not an important fact to report, then you’re in complete denial) didn’t the authors tell us what was going-on on Day-8? Were the colonial forms already present? Why don’t they tell us, one way, or the other. This paper, in NO WAY, ‘discounts’ chemical induction.

I assume that you are referring to the 1993 Hessen & van Donk paper. I am at somewhat of a disadvantage, since I can’t seem to access that paper online, but from other papers that reference it that I can get access to, you seem to be misinterpreting it. For example, from the second paper you quote later in your post:

Lurling wrote:

Hessen and Van Donk (1993) discovered the involvement of a chemical cue released from the zooplankton in stimulation of colonies. The addition of filtered medium from a Daphnia culture (2 % v/v) to unicellular Desmodesmus subspicatus populations resulted within two days in populations dominated by colonies, while the controls remained unicellular.

Other papers, including at least one by the co-author van Donk, all indicate that it is within 48 hours that the colonies become dominant. None of them indicate a 3-5 day waiting period for the forms to appear.

Figure 2a has the data for Day 8. The data shows that colonial forms were present in low but growing quantities, according to the non-visual Celloscope. However, presence and appearance are two different things. The appearance of colonial forms in the visual microscopic samples was not reliable until Day 10.

The paper makes four arguments as to why induction is discounted. Here is the paraphrase of why the discounted it.

1. In induction, colony formation occurs and dominates quickly. This was not the case for this experiment.
2. In induction, colony formation is proportional to the density of the inducing substance. In the experiment, colony formation was independent of the flagellate density (for density>0).
3. In induction, colony formation is dependent on the continuing presence of the inducing substance. In the experiment, colony formation was independent of the continued presence of the flagellate.
4. In induction, colony formation is independent of available resources. In the experiment, colony formation was dependent on available resources.

The results of the experiment were consistent with known selection models and inconsistent with known induction models. Ergo, the induction model is discounted. Future experiments may someday discover an induction model that satisfies these requirements, but until then, the selection model is preferred due to its efficacy.

I’m tiring of all of this. I could easily go on and point out that what we see is best explained as a ‘mother cell wall’ phenomena; and to point out that ‘multicellularity’ is never really achieved or arrived at [although it’s the authors main thesis. At best, the cells just simply ‘cling’ to the mother cell walls, which themselves cling to one another]. But as I say, I tire of all the nonsense on this board.

Most of the nonsense is coming from you, blast. We are merely pointing out the obvious errors. If multicellularity is not achieved, what is your definition? Differentation is not being claimed here. Merely inheritable traits that cause multiple cells to cling together. And no-one disagrees (AFAICT) that the phenomenon involves the mother cell walls. What do you think the selection argument is trying to claim? Your objection is puzzling.

I’ll just leave you with this quote from a 2004 review article:
(Plant Physiology, January 2004, Vol. 134, pp. 1–2,)

“Colonies of Chlamydomonas and Chlorella spp. stimulated quorum sensing-dependent luminescence in Vibrio harveyi, indicating that these algae may produce compounds that affect the quorum sensing system in Vibrio species.”

No one is disputing that induction happens. We’re just disputing that induction is happening in this case.

And this quote from a 2003 review paper: (Phenotypic plasticity in the green algae Desmodesmus and Scenedesmus with special reference to the induction of defensive morphology, M. Lürling; Ann. Limnol. - Int. J. Lim. 39 (2), 85-101)

“In fact, in culture unicells may be very common (e.g. Hegewald 1982, Holtmann & Hegewald 1986, Lürling & Beekman 1999, Trainor 1998), even at cell density far above ca. 1000 cells.ml-1. Hence, low cell density (Egan & Trainor 1989b) does not seem a prerequisite for unicell development in several Desmodesmus and Scenedesmus strains.

And why are there that few reports of unicellular Desmodesmus and Scenedesmus from the field ? One explanation could be that due to the activity of grazers unicells are produced only in very low numbers, which experience a high mortality ; protective colonies are being induced. Trainor (1979) observed that unicells disappeared when incubated in dialysis sacks in the field or when cultured in pond water in the laboratory. Interestingly, in another study ten years later the same strain produced unicells in water from the same pond (Egan & Trainor 1989b,d). Perhaps the activity of grazers had been involved in this plasticity and grazer-associated chemical cues might account for the different observations by Trainor (1979) and Egan & Trainor (1989b,d). Also colonial D. abundans from the field formed unicells in the laboratory (Fott 1968). Another reason may be that unicells are simply not recognized as Scenedesmus. Opening a textbook one will find Desmodesmus and Scenedesmus presented as «a freshwater colonial green alga» often supported with images of four-celled coenobia. Unicells may resemble species described in at least eight other green algal genera (Trainor 1998). Kessler and co-workers using sequence analyses of 18S rDNA showed that two taxa of the unicellular Chlorella were in fact unicellular Scenedesmus while one Chlorella and one Kermatia had to be designated to Desmodesmus (Kessler et al. 1997)!!!!

And the point of this (other than demonstrating that you already knew that induction occurred within 48 hours) is what? It does not support your induction claim. Best as I can tell, it demonstrates that the cladistics for algae were wrong because the cladists didn’t realize the plasticity of certain algae’s forms.

Adieu.

Somehow, I doubt it.

Comment #88320

Posted by W. Kevin Vicklund on March 21, 2006 6:53 PM (e)

The fact that two ‘taxa’ of Chlorella have been shown to actually be Scenedesmus, which is known to form a 8-cell colonial form through chemical induction, doesn’t seem to slow you down one bit, does it? Just pretend I never pointed it out.

Demonstrate that this particular species of Chlorella is actually Scenedesmus. But that would be even more devastating to your argument, since the characteristics of the known inducements for Scenedesmus are contradicted by the evidence.

Comment #89328

Posted by Anton Mates on March 26, 2006 3:53 AM (e)

Kevin and Pim have refuted most of Blast’s closing arguments–though several of those arguments more or less refuted themselves. (Chlorella colonies aren’t multicellular, they’re just a bunch of cells that stick together? We’re entitled to ignore peer-reviewed articles if they contain synonyms? I see…) There’s just a couple of things I wanted to add.

First, although it’s already been pointed out several times, the Scenedesmus chemical induction phenomenon Blast referenced was cited in this very paper (Hessen & Van Donk 1993 was the initial study published on it so far as I can see) and provides the very example of induction Boraas et al. contrast against their own observations! The authors’ four arguments against induction were provided precisely to show that these two appearances of colonialism are not attributable to the same mechanism. Why Blast went to the trouble of finding more papers on Scenedesmus when no one’s disputing that that phenomenon really is induction, I’m not sure.

Second, one of the above anti-induction arguments is that the Chlorella colonies took much longer to appear after the flagellate’s introduction (20-100 generations) than we would expect if they were chemically induced. Blast counters that that duration can be accounted for if you add in some extra time while the colonies “multiply and become evident:”

So, they first say that ‘colonies’ did not become apparent for about 20 Chlorella generations. But if the ‘multicells’ are dominant for the first month, then that means the growth rate of the ‘colonies’ will be less (perhaps much less) than that of the ‘multicells’. And since to ‘conservatively’ rule out chemical induction we’ve taken the 5-day mark as the time of the ‘trigger’; and since the authors tell us that on day 10 the ‘colonial’ forms were seen, that means that to determine the number of generations involved in the colonial forms appearance, we divide the 5 days by the growth rate.

Unfortunately, this stuff about growth rates is pretty much useless for explaining the observations under an induction model, because you wouldn’t need to wait for the colonies to multiply in order to see them. In an evolutionary scenario, the growth rate would matter–all colonies will be descended from one or a few mutants, so you have to wait around while that small population grows large enough to be spotted. But in an induction model, lots of unicells are each giving rise to colonies–that’s the whole point of induction, after all! It doesn’t matter how slow the colonies reproduce; there should be plenty of first-generation colonies, immediate descendants of unicells, to be evident under the microscope.

So Blast’s explanation fails, and the the long duration before colony appearance remains good evidence (along with the true breeding of colonies, and the independence of colony number from flagellate density, and the suppression of colonies when the culture was darkened) that this wasn’t induction.

Wow, is the thread really over? I’m almost regretful…

Comment #97422

Posted by Jason on April 19, 2006 6:10 PM (e)

Jebus! I can’t believe this crap went on for a month or more!

Will someone please explain to me how, if the Chlorella were becoming a new species, did it become the same species over and over again?

IOW, when the single-celled species was put under the same pressures, it rapidly evolved into a brand new species, and did it repeatedly 70% of the time.

Is this an accurate description of what happened, in your opinion?

Comment #97489

Posted by W. Kevin Vicklund on April 19, 2006 9:11 PM (e)

First, I don’t know if the differences are enough to truly classify it as a separate species. It’s one of those fuzzy areas in biology when it comes to these types of critters.

Secondly, we haven’t determined whether this is a series of identical (or similar) mutation events that has arisen in most of the experiments, or if this is a persistent subpopulation that is below detection levels. The data as given supports both hypotheses. If the first, it would indicate that the mutation leading to colony formation is quite easy to obtain, which to me points to either a single point mutation or the wild-state being unstable but highly selected (ie multiple sites where a mutation can lead to colony formation). I think I’d favor the unstable explanation, as it better explains the multitude of colony sizes at first.

Comment #97587

Posted by Anton Mates on April 20, 2006 10:49 AM (e)

I think I’d favor the unstable explanation, as it better explains the multitude of colony sizes at first.

As would I, for the same reason. Evidently many different mutations were possible, given the initial explosion of colony sizes, so it seems unlikely that only one of them would result in 8 cells. Indeed, it’s hard to think of any phenotypic change that could only be accomplished by one possible mutation. If nothing else, codon redundancy means that two or three different mutations could result in precisely the same protein. And since a couple of fairly simple physical changes were responsible for multicellularity–incomplete breakdown of mother cell walls and adhesion of daughter cell walls–it’s likely that there’s many related proteins that could pull those off.

The “variable morphologies” of the 8-celled colonies also suggest that the genetic mechanism for multicellularity wasn’t exactly the same in every lineage. And if there was a pre-existing permanent 8-celled population, we would expect it to take over immediately upon flagellate introduction, rather than only appearing after a couple of population crashes and the subsequent appearance of various other colony sizes.

Jason, the reason the Chlorella ended up evolving into what was, at least to our eyes, very similar morphs* 70% of the time, was that they were subjected to exactly the same selection pressure each time. Anything with under eight cells got eaten, anything with eight cells or more was predation-free, but anything with over eight cells was much worse at taking up nutrients. So there was a very strong selection pressure each time for the same sort of phenotype, no matter what particular mutation caused it.

You see a similar phenomenon in human malaria resistance. There’s a bunch of mutations which confer resistance to malaria, and they all work differently–but since the malaria parasite lives in red blood cells, most of them affect those cells somehow. As a side effect of that, they tend to cause anemia. So even though we don’t expect the same precise mutation to arise every time, it’s a good bet that a human population that’s lived for a long time in a malaria-prone region will have a high incidence of some kind of genetic anemia.

*Like Kevin says, “species” are hard to define for asexual organisms, although I’d be happy to call this a new species. They’re typically defined on much less blatant morphological differences than this, plus the colonial and unicellular population can stably live side by side, forming an ecosystem with the flagellate. Should each 8-celled variant be considered a different species if it’s genetically distinct? Probably not, simply because then we’d have to call almost every asexual lineage a separate species. Better to reserve the term for when a genetic difference is accompanied by a significant morphological and ecological shift.