Historical contingency in the evolution of E. coli

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While I was traveling last week, an important paper came out on evolution in E. coli, describing the work of Blount, Borland, and Lenski on the appearance of novel traits in an experimental population of bacteria. I thought everyone would have covered this story by the time I got back, but there hasn't been a lot of information in the blogosphere yet. Some of the stories get the emphasis wrong, claiming that this is all about the rapid acquisition of complex traits, while the creationists are making a complete hash of the story. Carl Zimmer gets it right, of course, and he has the advantage of having just published a book(amzn/b&n/abe/pwll) on the subject, with some excellent discussion of Lenski's work.

The key phrase is right there at the beginning of the title: historical contingency. This paper is all about how accidents in the genetics of a population can shape its future evolutionary trajectory. It is describing how a new capability that requires some complex novelties can evolve, and it is saying plainly that in this case it is not by the fortuitous simultaneous appearance of a set of mutations, but is conditional on the genetic background of the population. That is, two populations may be roughly equivalent in fitness and phenotype, but the presence of (probably) neutral mutations in one may enable other changes that predispose it to particular patterns of change.

Here, read the abstract for yourself, paying special attention to the parts I've highlighted.

The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E. coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit(+)) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. The long-delayed and unique evolution of this function might indicate the involvement of some extremely rare mutation. Alternately, it may involve an ordinary mutation, but one whose physical occurrence or phenotypic expression is contingent on prior mutations in that population. We tested these hypotheses in experiments that "replayed" evolution from different points in that population's history. We observed no Cit(+) mutants among 8.4 x 1012 ancestral cells, nor among 9 x 1012 cells from 60 clones sampled in the first 15,000 generations. However, we observed a significantly greater tendency for later clones to evolve Cit(+), indicating that some potentiating mutation arose by 20,000 generations. This potentiating change increased the mutation rate to Cit(+) but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection.

What Blount et al. are doing is testing SJ Gould's old claim that if we replayed the tape of life, we would not get the same results each time. Each step in evolution is dependent on prior history — it is contingent — and since many of the steps are driven by chance yet unfiltered by selection, we cannot predict the direction of evolution.

We can't rewind the whole planet, but with careful design, we can set up populations that can be rewound. Lenski has done this by setting aside 12 separate populations of E. coli 20 years ago, each one evolving independently and in its own direction. So far, over 44,000 generations have passed in the flasks in Lenski's lab. This is a long time, and at the typical mutation rates present in these creatures, it means that every nucleotide has been mutated singly multiple times in the population — in other words, there has been ample time to thoroughly explore the single substitution search space. In addition, a sample of each population was taken and frozen every 500 generations, so they can go back in time at will and examine their genome or even restart the line. Imagine what we could learn if some ambiguously benevolent space aliens had visited the earth every 5-10,000 years, snatched up a couple of random hominin/primate tribes, and had them tucked away in cryogenic storage — that's what this experiment is like.

These bacteria have been raised in a constant environment, one which is somewhat less than ideal: they've been fed on small quantities of glucose, and nothing but glucose, in a lean regimen that has encouraged selection for somewhat different properties than you'll find in your gut, one of the normal habitats of E. coli. They have evolved, and even have distinctive morphological characters, and many of their properties are consistent from population to population. There is one property that would be useful for the bacteria, but that has evolved in only one of the 12 populations: the ability to use citrate as a carbon source. There's plenty of citrate in the medium, and it would be a bit of a coup for any bacterium to acquire the ability to take up and metabolize it, but it just hasn't happened as often as might be hoped…except in one of the 12 populations, which around the 33,000th generation, suddenly expanded its stable population size by exploiting citrate in its environment.

How did that happen? As the abstract states, they were testing two alternatives. In one, the new ability is purely the product of an extremely rare mutation, some unlikely combination of events that gave a fortunate individual in this population the ability to take up and use citrate. If this were the case, and we rewound the tape of E. coli history back to before the mutation arose, and allowed it to play forward again, we'd expect no enhanced likelihood of a repeat performance — it's just like the other 11 populations. The other alternative is that the population had some prior enabling characteristic, some quirk in its genome that didn't really affect survival in one way or another, but that, in combination with some other ordinary mutation of ordinary probability, could predispose the population to acquire the useful citrate characteristic. In this case, rewinding the tape of life back to before the appearance of the ability, and re-running it forward, would show an increased frequency of reappearance of the ability. Furthermore, by running the tape back further still, they can identify when the enabling change in the population first arose.

The citrate+ trait was first observed in the population called Ara-3 at roughly generation 33,000. By looking back at the frozen populations, they determined that the initial mutation that enabled growth on citrate actually appeared sometime between generation 31,000 and generation 35,000. These early generations were not as efficient at growing on citrate, so another mutation is thought to have occurred around generation 33,000 that allowed much more rapid growth. E. coli from generations prior to 31,000 had no significant, detectable ability to grow on citrate.

So they pushed it back further, by taking samples from earlier generations and allowing them to replicate again, replaying history. If the citrate mutation was a rare, unique mutation, they wouldn't expect to see the novel trait arise again. What they saw, though, was that the bacteria sampled after the 20,000th generation re-evolved the citrate capability with a greater frequency — there is something that arose around generation 20,000 in the Ara-3 population that did not make them citrate+, but did make it easier for subsequent generations to evolve citrate+, confirming their hypothesis of a historical contingency.

This is the lesson: the likelihood of certain mutations arising is strongly affected by historical contingencies — different populations will have different probabilities of producing a particular trait. There were at least 3 events in the history of this one population of E. coli that enabled growth on citrate. The first was an enabling variation at around generation 20,000; the second was an initial mutation that actually allowed slow citrate uptake at around generation 31,000; and the third was a refinement at generation 33,000 that made the bacteria grow much better on citrate. Note: 3 mutations had to occur to produce the visibly better growing citrate+ population.

The creationists are already leaping all over this result and garbling and twisting it hopelessly. Michael Behe was quick to claim vindication, saying that these results support his interpretation.

I think the results fit a lot more easily into the viewpoint of The Edge of Evolution. One of the major points of the book was that if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it. But if more than one is needed, the probability of getting all the right ones grows exponentially worse. "If two mutations have to occur before there is a net beneficial effect — if an intermediate state is harmful, or less fit than the starting state — then there is already a big evolutionary problem." And what if more than two are needed? The task quickly gets out of reach of random mutation.

Wait a minute — has he read the paper? This is an experiment that revealed a trait that required at least three mutations. Yet there it is, produced by natural evolution, with no intelligent design required; and when the experiment is re-run with populations that had the initial enabling variant, they re-evolved the ability multiple times. It seems to me that this work demonstrates that drift, chance, historical contingency, and selection are sufficient to overcome his "big evolutionary problem", and directly refute the premise of his book.

If the development of many of the features of the cell required multiple mutations during the course of evolution, then the cell is beyond Darwinian explanation. I show in The Edge of Evolution that it is very reasonable to conclude they did.

This is simply baffling. Behe claims that he has shown in his book that the result observed by Lenski and colleagues could not occur without intelligent intervention…yet it did. He is trying to argue that an experiment that showed evolution in a test tube did not show evolution in a test tube. Behe's claims are comparable to someone living after the time of Kepler and Newton trying to claim that because Copernican circular orbits don't fit the data cleanly, the earth must be stationary — in response to research that shows the earth is moving. That is how backward Behe's claims are.

Behe is a bad note to end on, so let's look at the paper's conclusion. The answer does not lie in an imaginary designer, but in the reality of historical variation. And this is a lovely discovery.

…our study shows that historical contingency can have a profound and lasting impact under the simplest, and thus most stringent, conditions in which initially identical populations evolve in identical environments. Even from so simple a beginning, small happenstances of history may lead populations along different evolutionary paths. A potentiated cell took the one less traveled by, and that has made all the difference.

(Crossposted to Pharyngula)


Blount ZD, Borland CZ, Lenski RE (2008) Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proc Natl Acad Sci U S A 105(23):7899-7906.

3 TrackBacks

While I was traveling last week, an important paper came out on evolution in E. coli, describing the work of Blount, Borland, and Lenski on the appearance of novel traits in an experimental population of bacteria. I thought everyone... Read More

One of the canards used by my fellow Christians who actively fight against the idea of evolution is that it can’t be proven because it can’t be observed. Scientists are observing evolution in carefully conducted tests that challenge some o... Read More

And deserved it is, in this remarkably ignorant article by a creationist named Peter Heck. It starts out very, very badly. It never ceases to amaze me how intellectually condescending evolutionary naturalists can be. Keep in mind, these are... Read More

241 Comments

Behe must now admit that he was completely wrong or lose all credability. Random mutation produced all three mutations necessary for the evolution of a new beneficial trait. This is exactly the example that he asked for, the documentation of every mutation in the step-wise process along with population sizes and selection coefficients.

The problem with the God of the gaps approach is that the gaps keep getting smaller. Pretending the gap still exists will not save Behe now.

Nitpick time:

When you said, “This is the lesson: the likelihood of certain mutations arising is strongly affected by historical contingencies”

What you meant to say was

“This is the lesson: the likelihood of certain substitutions occurring is strongly affected by historical contingencies.”

Behe has no credibility, not as a scientist anyway. Perhaps he’s more credible than Ken Ham. On second thought, no.

What is incredible, though, is that Behe states the conclusion of the research, then in breathtaking inanity creates a “just so” story that supports his hallucination.

Maybe that’s why he’s a creationist; he just creates stuff.

I would think that the likelyhood of a mutation(substitution) occuring would be independent of the genotype, but the likelihood that a mutation would be benificial and fixed would be.

Reed A. Cartwright said:

Nitpick time:

When you said, “This is the lesson: the likelihood of certain mutations arising is strongly affected by historical contingencies”

What you meant to say was

“This is the lesson: the likelihood of certain substitutions occurring is strongly affected by historical contingencies.”

A related finding from a recent hosing of a creo on pharyngula. By selecting bacteria to utilize a novel sugar, scientists have been able to observe gene duplication followed by mutation/divergence. Which is what everyone has been saying for decades.

Doesn’t matter, the creos just move the goal posts again. Already we are hearing that if scientists can’t product a Big Bang in the laboratory to create a new universe, that it must not have happened. This the ultimate in unfalsifiability. If they did, there would be no one left alive to write up the paper or read it.

movethegoalposts: If you are claiming that research has been proven to show that gene duplication creates new functional genes that have NOT been previously found in an existing organism, please cite your paper. Otherwise, it’s just empty claim.

Xylitol is also not normally metabolized, but Mortlock and his colleagues were able to develop strains (generally through spontaneous mutations, but sometimes with u.v. ray or chemical induced mutations) that could use it because ribitol dehydrogenase (which is usually present in the cells to convert ribitol to D-ribulose) was able to slightly speed up the conversion of xylitol to D-xylulose, for which metabolic pathways already exist. The ability of the strains to utilize xylitol was increased as much as 20 fold when first production of ribitol dehydrogenase was deregulated (the enzyme was produced all the time, not just when ribitol was present), then duplication of the ribitol dehydrogenase genes occurred, then the structure of the enzyme was changed such that its efficiency at working with xylitol was improved, and finally, in at least one case, a line regained control of the modified ribitol dehydrogenase gene so that the enzyme was only produced in the presence of xylitol. Here we have a complete example of a new metabolic pathway being developed through duplication and modification of an existing pathway.

Actually we have seen duplication followed by mutation in at least one model system. So much for whereismysanity. So it isn’t an empty claim. Time to move the goal posts once again. Or maybe realize that evolution is a fact and theory. No doubt which way he will go.

You guys have been doing this for thousands of years now. First it was Zeus and Apollo Helios. Then it was the flat earth followed shortly by geocentrism. Then it was creationism. Some people never gave up any of those.

Was the citrate a part of the growing medium, or was it produced through glucose metabolism?

I’m not a Yank a Yank a [omitted for diplomatic purposes] tank but will attempt a bash at the history of those erudite and exceptional peoples. What if A. Lincoln’s son, Robert, hadn’t failed an entrance examination to Harvard, prompting his father to to visit him - and, Father, in need of $200, accepted a lecture engagement to coincide with visiting his son. This lecture, staged in New York, was pivotal in setting Lincoln on the road to the presidency.

The republican nomination battle for Illinois then happened to be carried in Lincoln’s favour through the showmanship of one R.J. Oglesby, who arranged for two old fence palings split by Lincoln to arrive on stage at a pivotal moment.

Then we have the legendary failure of a printer to deliver tally sheets by 9pm on the night of the deciding vote, Chicago, 1860. The vote was adjourned - and the foregone conclusion of who would become the republican nominee was turned on its head over the time space of a few hours.

Fate? Predestination? A confluence of environmental factors? This is one of the mysteries of the Universe. One can speculate until the big crunch renders speculation unnecessary.

What would have become of Man, if horses, dogs, sheep, cattle, and flowering plants hadn’t happened put in an appearance at the appropriate moment in geologic time?

R. Owen pointed out such obvious facts before Darwinism, and deduced that something along the lines of “pre-ordination” was at work.

That doesn’t mean that the “pre-ordination” empirically establishes the existence of a “Pre-Ordinator” in a test-tube. Neither does the pursuit of nature study require any particular religion. And “pre-ordination” doesn’t rule out environmental happenstance and response to environmental happenings.

One can argue over chance, fate, and pre-ordination, forever - but there can be no removal of any one of those possibilities from the science scene - including pre-ordination. Rapidly morphing microbes of hazy descent and classification that obviously respond to environment and are seemingly an accident of history aren’t entirely novel and are a standing testimony to the way the universe functions. That’s life. They couldn’t respond to environment and pick up a programming factor during the course of their existence if there wasn’t a technology furthering the procedure. Science’s task is to find the technology, not merely to catalogue something and then provoke an argument over chance vs. pre-programming.

PBH has been drinking again I see :)

Great paper PZ, thank you for explaining in terms we layman can appreciate.

The citrate+ trait was first observed in the population called Ara-3 at roughly generation 33,000. By looking back at the frozen populations, they determined that the initial mutation that enabled growth on citrate actually appeared sometime between generation 31,000 and generation 35,000.

Shouldn’t that last 35,000 be 33,000? (The mutation presumably appeared before the observed enhanced growth.)

(Behe) “If two mutations have to occur before there is a net beneficial effect — if an intermediate state is harmful, or less fit than the starting state — then there is already a big evolutionary problem.” And what if more than two are needed?

But that’s only if those specific mutations are the only way to reach the particular beneficial trait that is being discussed.

And of course, the remark that somebody always has to say to articles like this one: It’s still E. Coli!!!111!one-eleven!!! :p

Henry

p.s. “Behe” and “Coli” aren’t in the spell checker.

Henry J said:

p.s. “Behe” and “Coli” aren’t in the spell checker.

And yet, Escherichia is.

How odd…

Test… Salmonella check Proteus check Flavobacter not in.

HDX,

I would think that the likelyhood of a mutation (substitution) occuring would be independent of the genotype, but the likelihood that a mutation would be benificial and fixed would be.

If the effect of the mutation depends on it happening in a particular allele, the likelihood would depend on the frequency of that allele in the population. I’m not sure if that’s independent of the genotype, or not?

Henry

Not too long ago panselectionists were citing these experiments as proof of the all-dominating powers of natural selection. Which is funny because there has always been a drift component in taking only a sample of survivors, instead of just pouring the next round of glucose over all surviving bacteria. Without this repeated founder effect, populational fixation of any mutation would probably be much, much slower. Natural selection alone is simply much less effective when it comes to accumulating a potentially adaptive “string” of mutations.

I also find very interesting that the citrate-eaters had “ups and downs” in their populational frequencies rather than a simple story of steady increase. Competition simply was not sufficient to eliminate the existence of these “minorities”, even though they could be described, in function of their lower frequency, to be “less fit” or “not-so-well-adapted”. Yet there they were.

Alexander Vargas said:

Without this repeated founder effect …

I doubt you get a founder effect when you reseed the next day’s cycle with billions of individuals.

HDX said:

I would think that the likelyhood of a mutation(substitution) occuring would be independent of the genotype, but the likelihood that a mutation would be benificial and fixed would be.

A substitution is a mutation that got fixed.

This was a “Holy Crap” paper, the kind you only see once every few years. Papers like this are why I love science.

PBH wrote:

“They couldn’t respond to environment and pick up a programming factor during the course of their existence if there wasn’t a technology furthering the procedure. Science’s task is to find the technology, not merely to catalogue something and then provoke an argument over chance vs. pre-programming.”

But they in fact did exactly that. Your hypothesis is conclusively falsified. Unless of course you can demonstrate this “technology” and how it operated in this experiment. Come on Phil, here is your big chance. You can run this exact experiment yourself and prove to everyone exactly what mechanism you are yapping about. It is your task to “find the technology” and yours alone.

Of course, until you provide some evidence, random mutation and natural selecetion, (demonstrable processes that are fully capable of producing this result), are all that is required. There were no photons “processed” in a magnetic field, no “information technology”, no intelligence in the sun directing the bacteria to be better, no poof miracles, just good old evolution in action. Once again, you were completely wrong. Just admit it and go away.

Behe seems to have turned off comments to his posting.

PvM said:

Behe seems to have turned off comments to his posting.

Sure, that’s what liars do when they are too chicken to let themselves by exposed on their own territory.

I love these kinds of papers because they are so real and are something a physicist can really identify with.

These creationists demand a repeatable, molecule-by-molecule reenactment of a stochastic evolutionary process before they will believe it, and yet this very demand betrays their profound ignorance of these processes and how they are studied by working scientists.

It’s getting harder and harder for me to believe that Behe was ever a real working scientist. And Lehigh’s Biology Department disclaimer about Behe’s claims becomes even more significant the more Behe sticks his flagellating hoof in his mouth.

I don’t find Behe that baffling. He’s basically saying predestination + unlikelihood-of-any-one-outcome = design. As always. Apparently his need for God’s need to make humans is so ingrained, he can’t see how it colors his thinking. As long as I can remember, creationists have argued “X just happened, and X is virtually impossible”, ignoring that the same is true of a shuffled deck of cards. The confusion is between “we can assume X, since we know it happened”, and “we could have assumed X, in principle, at any point in history”

Wow. I’m used to biologists thinking in terms of generations and deep time by now, but 20 year experiments seems pushing it.

It’s still E. Coli!!!

Is it?

The biologists will set me right here, but species is a human description of different populations, and as for bacteria it seems to me an ecological description makes much sense. (As for example the recent paper I’ve mentioned in another thread, where sea water bacteria populations were most easily separated by sequencing and evolutionary ecological modeling in combination.)

I’m reasonably sure that you now could set up an environment where a population of the citrate+ strain will be able to survive in but not the native one that prefers your gut. That would be speciation by the ecological criteria, wouldn’t it?

“Behe” and “Coli” aren’t in the spell checker.

If one goes, they should both go - seeing as they are organisms that likes to make shit up.

Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5882-6. Links Adaptive evolution that requires multiple spontaneous mutations: mutations involving base substitutions.Hall BG. Biology Department, University of Rochester, NY 14627.

A previous study has demonstrated that adaptive missense mutations occur in the trp operon of Escherichia coli. In this study it is shown that, under conditions of intense selection, a strain carrying missense mutations in both trpA and trpB reverts to Trp+ 10(8) times more frequently than would be expected if the two mutations were the result of independent events. Comparison of the single mutation rates with the double mutation rate and information obtained by sequencing DNA from double revertants show that neither our classical understanding of spontaneous mutation processes nor extant models for adaptive mutations can account for all of the observations. Despite a current lack of mechanistic understanding, it is clear that adaptive mutations can permit advantageous phenotypes that require multiple mutations to arise and that they appear enormously more frequently than would be expected.

There is a lot of data that contradicts Behe’s fallacies of more than 2 mutations are impossible. Here is one such paper.

Another is below. This model system starts with a deletion of the beta gal. gene, which hydrolyzes lactose. These E. coli strains are then selected which evolve a new beta gal., ebg=evolved beta gal. This requires 2 mutations since a repressor regulates the ancestral operon. In one case, by sequencing they found a triple mutation.

1: Genetics. 1989 Dec;123(4):635-48. Links

Erratum in: Genetics 1990 Mar;124(3):791. DNA sequence analysis of artificially evolved ebg enzyme and ebg repressor genes.Hall BG, Betts PW, Wootton JC. Molecular and Cell Biology, University of Connecticut, Storrs 06268.

The ebg system has been used as a model to study the artificial selection of new catalytic functions of enzymes and of inducer specificities of repressors. A series of mutant enzymes with altered catalytic specificities were previously characterized biochemically as were the changes in inducer specificities of mutant, but fully functional, repressors. The wild type ebg operon has been sequenced, and the sequence differences of the mutant enzymes and repressors have been determined. We now report that, contrary to our previous understanding, ebg enzyme contains 180-kD alpha-subunits and 20-kD beta-subunits, both of which are required for full activity. Mutations that dramatically affect substrate specificity and catalytic efficiency lie in two distinct regions, both well outside of the active site region. Mutations that affect inducer specificity of the ebg repressor lie within predicted sugar binding domains. Comparisons of the ebg beta-galactosidase and repressor with homologous proteins of the Escherichia coli and Klebsiella pneumoniae lac operons, and with the galactose operon repressor, suggest that the ebg and lac operons diverged prior to the divergence of E. coli from Klebsiella. One case of a triple substitution as the consequence of a single event is reported, and the implications of that observation for mechanisms of spontaneous mutagenesis are discussed.

The theory for this is that organisms under stress due to selection may show a higher mutation frequency as bursts of mutagenic polymerases are produced or DNA repair mechanisms become overwhelmed or dysfunctional. Not sure if the mechanisms are known too well.

Behe’s theories are equivalent to proving that bumble bees can’t fly with mathematical aerodynamic modeling. The problem with that theory is that bumble bees do fly. As Feynman and others have pointed out, many a beautiful theory has been ruined by an ugly fact.

panselectionists

Hello Sanders. As you will pontificate on that Dawkins is a nincompoop dodo together with that natural selection is complete crap countless times, why don’t you get both interminable contrafactual themes started at the same time. The suspense is killing me … not.

I doubt you get a founder effect when you reseed the next day’s cycle with billions of individuals.

And didn’t they control for that, as they could precisely repeat the part of the experiment where the necessary mutations arose?

Wow! Mountains from molehills! This sort of change is called “micro-evolution I recall and no one doubts it. Are these population still bacterium? Yep!

Moreover, I’d be interested in James Shapiro’s take on the actual mechanism since he is not a complete dolt like Pee Wee and has established for bacteria rapid change mechanisms having essentially nil to do with RM and NS.

So he wouldn’t have to use doublespeak BS like NEUTRAL mutations that cause change, predisposition to change, blah, in direct contradiction to the definition of same.

All hat and no cattle with this guy.

Behe’s nonsense depends on a lot of hidden asumptions. Hidden because he doesn’t care enough to read the literature or learn anything about science.

If one starts selecting spontaneous mutations, it doesn’t take long to pick up “mutator phenotypes.” These are strains that have mutations in DNA replication and repair enzymes and higher mutation frequencies. These are common and known for many genes.

So really what you were selecting for is bacteria with higher mutation frequencies which then yield the mutations one was selecting for.

With mutator strains, his numerology crashes big time. But data like this is never a problem for creo crackpots. They just ignore it, wave their hands, or move the goal posts. This is neither honest nor science.

keith said:

All hat and no cattle with this guy.

Project much?

And when’s that debate going to happen? You know, the one between Dembski and Dr. Elsberry that you’re setting up and funding?

Right on time, the troll Keith jumps in.…

Wow! Mountains from molehills! This sort of change is called “micro-evolution I recall and no one doubts it.

Nope, just Mountains.

Once again, though you whine mightily about the shibboleth of “microevolution”, you never explain the difference between your mystical microevolution and just plain evolution, nor do your ilk ever posit a limiting mechanism.

It’s like whining that there exists such a thing as micromath and macromath, and just because nobody has lived long enough to see a human being start from zero and count to a million then it’s impossible to have numbers that big.

There is no micromath, troll, there is just math and there is just evolution.

If there is, put your cards on the table, just what do you propose as the limiting mechanism, troll?

Your entire argument rests on the idea that there is some magical mechanism that prevents a man from walking across the state because he has only demonstrated he can walk across the town. This despite the fact that there are footprints all over the planet.

Are these population still bacterium? Yep!

Yep! And you, the dog curled up at your feet, and the burger you had for lunch, are still all chordata. What is your point?

Whistle past the cemetery all you want, troll, but on a bacterial scale, this is the much vaunted “dogs turning into cats” that your ilk is always whining about.

Thats a new one to me. I would call insertions, deletions and substitutions as mutations whether they are fixed or not. An insertion mutation that is fixed is not called a substitution.

Reed A. Cartwright said:

HDX said:

I would think that the likelyhood of a mutation(substitution) occuring would be independent of the genotype, but the likelihood that a mutation would be benificial and fixed would be.

A substitution is a mutation that got fixed.

HDX said:

Thats a new one to me. I would call insertions, deletions and substitutions as mutations whether they are fixed or not. An insertion mutation that is fixed is not called a substitution.

Yeap, its a common misconception to think that substitution=point mutation. I blame it on the protein guys that only compare differences between species.

If you only ever look between species, then the differences you see will be substitutions because they will have been fixed.

And yes, although they are rarely described as such substitutions can be indels, translocations, etc.

I said

“there has always been a drift component in taking only a sample of survivors, instead of just pouring the next round of glucose over all surviving bacteria”

This is, of course, an extra step that is regardless of the sample size.

If you can’t understand why this part of the protocol is not the same as natural selection, well, I can’t help you.

Larsson: when someone says selection is not everything, or that selection is not the main mechanism, he is not saying selection is total crap. This is on the accout of your panselectionist paranoia. Selection (an importnat factor of evolution) must be put in perspective rather than abusing it like an amateur to explain anything.

Unfortunatley, amateurs are very prone to this becuase they are misled by people like Dawkins into thinking that if they understand selection, they understand evolution. Further they are fooled into believeing this is the only way we can say evolution is “explained” such that without it we’d be the happless victims of creationists.

The result is that amateurs will point to any evolutionary process and say “natural selection”. This is just sad, since evolutionary biology should not be distorted in function of looming creationism.

FWIW, catching up on old threads.

Alexander Vargas said:

Maybe some other day you will feel more inclined to discuss a little SCIENCE.

I have done science. What is your excuse for boring comments?

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