Andrea Bottaro posted Entry 1519 on October 16, 2005 11:15 PM.
Trackback URL: http://www.pandasthumb.org/cgi-bin/mt/mt-tb.fcgi/1515

Spurred by a host of new findings in molecular and cellular biology, in recent years an increasing number of determined biologists have come to envision processes that contradict century-old biological assumptions and seem to defy the expectations of Darwinian evolutionary theory…

Naaah, I am not talking about ID. I am talking about prions, the specter of Jean Baptiste de Lamarck, and “heretical” views about biology. And what must be truly baffling for conspiracy-minded ID advocates, the inflexible “Darwinist orthodoxy” seems to positively dig this “heresy”. Now, that must hurt…

For many years after their discovery as the agents of some rare neurodegenerative diseases in mammals, such as scrapie in sheep and human Creutzfeldt-Jakob disease and kuru, prions have remained a truly esoteric research topic. However, they have recently become well-known to the public as the cause of bovine spongiform encephalopathy, a.k.a. BSE or “mad cow disease”, which can be occasionally transmitted to humans causing variant Creutzfeld-Jacob disease (vCJD). (Information about prion diseases can be found at the web sites of the WHO and the National Prion Disease Pathology Surveillance Center.)

Prions are unlike any other infectious agent in that they seem to have no nucleic acids at all. Indeed, after a long controversy, most scientists currently agree that prions propagate entirely as alternatively folded forms of certain proteins, through a mechanism that resembles crystal nucleation (see figure below) [4,8,12].

prionssm.jpg

Prion formation and replication. Click on image for larger version.

In the neurological diseases mentioned above, a prion protein can cause a “normal” folded protein of the same type (called PrPc for prion protein - cellular form) to assume a prion-like conformation. (For a PT primer on protein folding and some recent findings, see here.) Misfolded prion-like proteins tend to form filaments, and cause conformation changes in additional PrPc’s they come in contact with. This results in an amplifying cascade that eventually leads to accumulation of prion protein fibers (“amyloid”) which cause progressive neuronal cell death, and ultimately disease manifestation. Transfer of prion proteins alone from a sick organism to a healthy one causes the propagation cascade to start anew.

Let’s pause here. Does something nag you? It should. When prions propagate, what gets replicated is not really a material entity. Non-pathogenetic, correctly folded PrPc proteins exist in a host before prion infection. Unlike all other infectious agents, prions do not make new forms of themselves by synthesizing anything. Like in the case of crystal formation, what gets replicated is a structure. In other words, prions are not replicating proteins, but replicating shapes in a protein substrate world. There is even evidence that the same prion may exist in alternative forms (“strains”) with different properties, which may potentially compete with each other for the available substrates (PrPc’s), in a sort of Darwinian competition between “immaterial” replicators. Now, this is not unexpected: Darwinain evolution is a logically unavoidable consequence of replicators displaying heritable variation in a selective environment. Nevertheless, it’s just spooky, if you ask me. But that’s not all.

People have found prions not only in mammals, but also in other organisms, such as yeast and other fungi. Fungal prions are a great system to study prion biology, because they can be manipulated in the lab without excessive concern with potential infectivity, and their host organisms replicate and express the prion phenotype very fast (unlike the lag time for prion disease symptom development in mammals). In addition, fungal prions have attracted considerable interest because they actually mediate heritable phenotypes in their natural hosts, phenotypes that in some cases can be adaptive.

For instance, a yeast prion called [PSI+] causes defects in protein synthesis termination, and formation of new proteins [10, 11, 6, 8]. As most of you know, ribosomes are the cellular organelles which assemble proteins by linking amino acids according to the nucleotide sequence of messenger RNAs. In a nutshell, [PSI+] prevents the ribosome from reading the RNA nucleotide triplets (codons) that encode for “stop” signals. This causes elongation of the encoded proteins past their normal stop sites (i.e., proteins acquire extra amino acid sequences at their tail end), or in some cases allows translation of pseudogene transcripts that are otherwise crippled by stop codons.

In normal conditions, this phenotype spontaneously appears at low frequency in yeast populations, and is unstable ([PSI+] cells can revert to normal at low rates). The [PSI+] phenotype is generally non-adaptive (in fact, mal-adaptive), but in certain conditions (for instance, if the environment changes drastically) some of the aberrant proteins it generates may confer advantageous new functions. If that happens, prion-bearing organisms capable of synthesizing the new advantageous proteins will spread through the population. These phenotypically altered cells, by surviving in the new conditions, have now a chance to acquire favorable genetic mutations through conventional mutation processes. If this happens, the gene mutation can take over the population, while the [PSI+] population is again counter-selected and essentially disappears.

The [PSI+] prion trait is transmitted in a non-mendelian fashion. When mating [PSI+] and [psi-] yeast strains, the progeny is [PSI+], and so are, counter to Mendel’s laws, all the progeny of this progeny (except for the low-frequency “reversion” rate to the normal phenotype). The possibility of generating the [PSI+] trait is genetically encoded in the sequence of the yeast gene for the normal version of the [PSI+] prion protein, called Sup35 (which has the ability to assume both prion and non-prion folds). Therefore, although the prion “option” is clearly subject to conventional Darwinian evolution, in the case of [PSI+] natural selection is acting on a non-mendelian, non-genetically encoded trait.

One of the most interesting aspects of these prion-dependent phenomena is that they seem to have evolved because they provide a “buffer” system against sudden environmental changes by allowing the rapid generation of large numbers of new phenotypes, one of which may turn out to be useful in the new selective conditions. Another mechanism with similar properties is the SOS response in bacteria, in which hypermutation occurs in environmentally stressful situations. “Evolvability” is an often misued term that refers to the evolutionary potential of certain traits or organisms, but it applies well in this case, to indicate the increased diversity of otherwise “hidden” phenotypes that are unmasked by the [PSI+] state [4-8].

Several scientists have also noted that prion-dependent phenotypes raise the very real possibility of specific direct environmental induction of a heritable phenotypic trait, a kind of Lamarckian evolution, or pre-programmed phenotypic switch [2-4,6,8,12]. In certain conditions, for instance when an organisms recurrently but unpredictably encounters a specific, strong selective condition, prion systems may result in the environmental induction of adaptive, acquired heritable phenotypes.

At this point, we don’t have any bona fide examples of this actually happening, but in principle it’s possible. Moreover, this model provides a real, testable mechanism to explain such a phenomenon, should it occur (scientists don’t mind testable mechanisms and hypotheses, even when they are “heretical”).
Aplysia_JPEG.JPG
In fact, something that comes tantalizingly close to this, at the cellular, if not organismic level, has been proposed to occur during long-term memory formation in the sea slug Aplysia californica[1,8,9]. This critter has been used experimentally for many years as a model for memory formation for its rudimentary learning processes and giant neurons. Long-term memory formation has been associated with the formation of stable functional contacts (synapses) between neurons, in a form of competition: many synapses form all the time, but only those that get progressively stabilized by repeated stimulation will persist. One of the proteins that has been associated with the synapse stabilization process in Aplysia is called ApCPEB. Its function is somewhat unclear but, like Sup35, it also may be involved in control of protein translation. ApCPEB localizes to the synapse region, and upon repeated synaptic stimulation it forms “clusters” with different regulatory properties compared to the monomeric protein. Once formed, these clusters remain stable despite protein turn-over, even in the absence of further stimulatory signals. In yeast, ApCPEB has been shown to act as a bona fide prion, which would explain the formation of clusters and their stable properties.

These findings have raised enormous interest, not only from prion specialists, but among biologists in general. Many papers have appeared in major journals discussing the data and their implications. The extent of these phenomena in the biological world is unclear: prion-based inheritance and evolution may be extremely rare, or perhaps it’s quite pervasive and we just missed it. Some scientists are already talking about “paradigm shifts” [e.g., 2], although that’s probably premature. Regardless, it certainly runs against the impression, which ID proponents are trying to project in their P.R. communiques, of a monolithic, censorial Darwinian orthodoxy bent on stifling dissent and hiding evidence inconsistent with mainstream evolutionary theory. It is hard to say at this point whether in 50 years evolutionary biology textbooks will devote prions a whole chapter, a page, or just a footnote. But prions, unlike ID, will most like be there.

References
1. Bailey CH, Kandel ER, Si K. The persistence of long-term memory: a molecular approach to self-sustaining changes in learning-induced synaptic growth. Neuron. 2004 44:49-57.

2. Bussard AE. A scientific revolution? The prion anomaly may challenge the central dogma of molecular biology. EMBO Rep. 2005 6:691-4.

3. Chernoff YO. Mutation processes at the protein level: is Lamarck back? Mutat Res. 2001 488:39-64.

4. Chernoff YO. Replication vehicles of protein-based inheritance. Trends Biotechnol. 2004 22:549-52.

5. Chicurel M. Genetics. Can organisms speed their own evolution? Science. 2001 292:1824-7.

6. Masel J, Bergman A. The evolution of the evolvability properties of the yeast prion [PSI+]. Evolution Int J Org Evolution. 2003 57:1498-512.

7. Partridge L, Barton NH. Evolving evolvability. Nature. 2000 407:457-8.

8. Shorter J, Lindquist S. Prions as adaptive conduits of memory and inheritance. Nat Rev Genet. 2005 6:435-50.

9. Si K, Lindquist S, Kandel ER. A neuronal isoform of the aplysia CPEB has prion-like properties. Cell. 2003 115:879-91.

10. True HL, Lindquist SL. A yeast prion provides a mechanism for genetic variation and phenotypic diversity. Nature. 2000 407:477-83.

11. True HL, Berlin I, Lindquist SL. Epigenetic regulation of translation reveals hidden genetic variation to produce complex traits. Nature. 2004 431:184-7.

12. Uptain SM, Lindquist S. Prions as protein-based genetic elements. Annu Rev Microbiol. 2002 56:703-41.

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Comment #52384

Posted by kay on October 17, 2005 5:13 AM (e)

So this is basically a virus-in-the-software-sense inside a biological system… very interesting read. Wonder how long it’ll take for creas to use it a straw man?

Comment #52385

Posted by Bo Johansson on October 17, 2005 5:55 AM (e)

And here is an illustration of what can happen when you make a successful hypothesis and present evidence that contradict century-old biological assumptions and seem to defy the expectations of Darwinian evolutionary theory…

Comment #52386

Posted by djlactin on October 17, 2005 6:12 AM (e)

One jangling bad note in an otherwise beautiful symphony:

“they seem to represent systems that have evolved to “buffer” against sudden environmental changes by providing a quick way … “

My graduate supervisor had me flogged for making teleological statements like this!

This type of statement “evolved to…” implies a purpose to evolution, a certain goal-directedness to evolution (shades of [shudder] an intelligence behind the process).

Traits don’t ‘“evolve to” do anything; they arise in a population randomly and then MAY spread if they confer an advantage to the bearer lineage: i.e., they evolve “because” they do something.

I suggest this as a better construction:
“they seem to represent systems that have spread throughout the population because they can provide a “buffer” against sudden environmental changes by providing a quick way…”

PUHLEEEZ don’t do this; it’s the kind of presentation that confuses the ‘lay’ reader and
fosters misunderstanding of the evolutionary process.

Comment #52387

Posted by K.E. on October 17, 2005 6:42 AM (e)

Or how long before the DI uses it hack their virus into the obedience software in the human mind. You have to give them credit though it is much easier to herd (group thinking) sheep than (free thinking) cats .

Comment #52389

Posted by Andrea Bottaro on October 17, 2005 7:05 AM (e)

djlactin - thanks for noticing that. I corrected it.

Comment #52391

Posted by Albion on October 17, 2005 8:07 AM (e)

Between viruses, prions, and autoimmune diseases, there’s a lot more out there to challenge “orthodox” germ theory than there is to challenge the theory of evolution. I wonder when the “evolution is an atheistic lie” crowd will do more than carp about HIV not causing AIDS and mount a full-blown attack on germ theory on the basis, perhaps, that a lot of diseases are really caused by sinful (or some carefully secular equivalent term) lifestyle.

Comment #52393

Posted by Ricardo Azevedo on October 17, 2005 8:51 AM (e)

It is interesting that the evolutionary implications of the PSI system, although proposed some 5 years ago, have never been rigorously tested using experimental evolution, although that would be relatively easy to do in yeast (the data in the 2004 paper also falls well short). I will have to reserve judgement on this mechanism until then: it is not enough that it sounds plausible. (Indeed, similar criticisms can be raised about the related claims on the evolutionary role of Hsp90 by the same lab.)

Comment #52394

Posted by Mike on October 17, 2005 9:05 AM (e)

Germ theory sherm theory. A prion is a chemical. Proteins are chemicals. I’m nearly certain that a toxicologist must have pointed out by now that if you don’t have any genes involved its kinda silly to be talking about inheritance. ***ITS A POISON***! Inheritance would come in when a gene encoding a protein that can do this is selected for, such as what you could invision happening with the fungal prion described above. Change the wording and you’ll see things in a more helpful context. Prions don’t infect, they contaminate. Its more than just non-mendelian, its non-genetic. The problem is that we’re not used to thinking of biological organisms as bags of chemicals. There’s still more than a little vitalism alive and kicking in biology.

Comment #52397

Posted by Andrea Bottaro on October 17, 2005 10:09 AM (e)

Ricardo:
I thought the 2004 Nature paper data were pretty good as far as determining the mechanism of action of [PSI+]. As for the role in evolution, I agree it’s largely speculative at this point. A recent paper in PNAS that I have not listed in my piece concludes that [PSI+] is not found in a number of wild yeast strains, suggesting that it may be deleterious overall (Nakayashiki et al, PNAS 102, 10575, 2005). If that’s the case, it is unlikely that this prion plays a significant role in determining yeast “evolvability” - although this may still be the case in specific environmental niches. Still, it’s an interesting phenomenon, well worth speculating about, in my opinion.

Mike:
Prions are indeed chemicals, but chemicals that, unlike poisons, reproduce themselves (in the unusual manner described above). Also, I should probably say that in the most basic meaning of the term “gene” (e.g., a physical unit responsible for stable inheritance of one or more phenotypic traits) prions are in fact genes of sort, although of course they do not fit the common, modern molecular definition of the term.

Comment #52401

Posted by Mike on October 17, 2005 11:23 AM (e)

Andrea Bottaro wrote: “Prions are indeed chemicals, but chemicals that, unlike poisons, reproduce themselves (in the unusual manner described above).”

But they aren’t actually reproducing themselves, are they? They are inducing a conformation shift in other protein molecules, something that some poisons do. Its not inheritance. The unique thing is that its acting in “cis”. Is there something other than entertainment value to be gained from insisting that this is a form of inheritance? It is still the genotype that must be altered in selection. Sorry to be a wet blanket, but I don’t get it.

Comment #52405

Posted by PaulC on October 17, 2005 12:23 PM (e)

“Now, this is not unexpected: Darwinain evolution is a logically unavoidable consequence of replicators displaying heritable variation in a selective environment. Nevertheless, it’s just spooky, if you ask me.”

The spookiness is probably a function of being a biologist having much more specific ideas about what kind of thing usually happens.

My intuition would be to look at this as a random graph (for lack of a more informed model). Suppose we have nodes labeled with pairs (X,s) representing a protein with sequence X and conformation s. The graph has directed edges labeled (Y,t) with endpoints (X,s) and (X,u). We interpret this as “X with conformation s will change to conformation u in the presence of Y with conformation t.” Any possible edge can be in the graph with some fixed (rather low) probability p.

Depending on the density of such a random graph, it would be downright spooky if we were miraculously prohibited from finding edges labeled (X,u) that go from (X,s) to (X,u). Not only that, the probability would likely be higher than our first guess, because it would look a lot like the birthday paradox (http://en.wikipedia.org/wiki/Birthday_paradox), i.e. the fact that in a room of 23 people the probability is better than 50% that two share a birthday.

Comment #52406

Posted by stevec on October 17, 2005 12:38 PM (e)

Mike,

These are abstract arguments, to be sure, but you could say that there’s a hint of vitalism in creating a distinction between gene inheritance and conformation inheritance. Both represent a self-replicating phenomenon; DNA has the property that a copy of its molecular arrangement happens under the right conditions, just as the prion induces new conformation copies in the presence of the normal protein. There’s no reason that selection couldn’t apply to the prion case, just as selection can happen to cultural phenomena. Selection simply needs a mechanism for replication of system states and variable probability of survival for different states. Natural selection occurs all the time in the replication of songs on teenagers Ipods.

Comment #52407

Posted by sanjait on October 17, 2005 12:39 PM (e)

“But they aren’t actually reproducing themselves, are they? They are inducing a conformation shift in other protein molecules”

They induce a conformation shift in other proteins, that results in more proteins of the same conformation. One could say that DNA/RNA do a similar thing, since they act as a template for the creation of a new macromolecule in the same “conformation.” The important aspect is that PSI+ is a phenotype passed from fungal parent to offspring.

Maybe another analogy would be an infection. Often a viral or bacterial infected organism passes it to the offspring. In many cases, this bacterial infecting agents act as symbionts, and at some point, the host often loses the ability to survive without them. Many creatures, like termites, use such a system for digestion. If the agent is viral, such as that which carries cholera toxin, the host is often adapted to reproduce with the virus. Often this results in permanent provirus status and incorporation to the genome.

The whole point is we have our simple model of inheritence, but when we see other mechanisms for which there exists evidence we embrace them enthusiastically, rather than hold onto them dogmatically as some have alleged. We can quibble about what defines words like “inheritance,” but when new discoveries challenge previous understandings in biology, we are bound to have to redefine.

Comment #52408

Posted by Mike on October 17, 2005 1:10 PM (e)

Well ok, just one more thing then I’ll shut up.

“There’s no reason that selection couldn’t apply to the prion case, just as selection can happen to cultural phenomena.”

What would be selected on in the case that is of primary interest to us, BSE? Nothing much in the cow. What might be selected against is the human stupidity of feeding a cow’s brain to a bunch of other cows. This cow prion, at least, hasn’t developed as a result of selection for one protein conformation to reproduce itself in other cows, unless there are zombie bovines that I’m unaware of. Isn’t this simply an example of a random event? One protein molecule conferring a conformation shift on another, a common event in protein-protein interaction, but this time there’s an extreme deleterious effect.

Would we be thinking of it in these terms if the people looking for it hadn’t been looking for an infectious agent?

Comment #52409

Posted by Andrea Bottaro on October 17, 2005 1:11 PM (e)

Just to add to the comments above. Prions do reproduce themselves (with the caveats described in my piece, i.e. that what reproduces is the protein fold, not the protein itself). If you inject an animal with a “poison”, as suggested by Mike, then transfer its tissues into an other animal, and so on sequentially, eventually you run out of poison and lose toxicity. Not so for prions. Second, the traits prions generate can be heritable in the “classic” sense - as in the case of the yeast prions, or some human forms of Cretzfeldt-Jakob disease.

Comment #52411

Posted by Russell on October 17, 2005 2:46 PM (e)

Would we be thinking of it in these terms if the people looking for it hadn’t been looking for an infectious agent?

Perhaps not. But the disease is, indeed, “contagious”, so it stands to reason that that is how it would first be approached. You can measure “infectious units” just like for other infectious diseases, and those infectious units multiply in an “infected” animal - just like they do for other infectious diseases. The fact that we use the language of infectious disease to describe the phenomenon is no more arbitrary or misleading than the use of the word “virus” for those nasty computer software constructs.

Comment #52412

Posted by jeebus on October 17, 2005 2:52 PM (e)

Prions do reproduce themselves… what reproduces is the protein fold, not the protein itself.

So, prions are just self-replicating quantum computers?

If so, could understanding (variation in) their machinery help us bring further insight to biochemistry’s (quantum physic’s) “protein folding” questions?

Comment #52413

Posted by Russell on October 17, 2005 3:25 PM (e)

By the way, there’s a suspicious cluster of CJ disease right now in Idaho

Comment #52415

Posted by Alan on October 17, 2005 4:17 PM (e)

I must be as dense as Mike here. The prion is not reproducing copies of itself. It is catalysing a deformation of an exisiting protein to the prion configuration. The protein which deforms exists anyway in the organism, and is, in effect, “poisoned” by being catalysed into the prion configuration. I don’t see any NS driving this. Sorry, if this is simplistic.

Comment #52418

Posted by PaulC on October 17, 2005 4:50 PM (e)

“I must be as dense as Mike here. The prion is not reproducing copies of itself. It is catalysing a deformation of an exisiting protein to the prion configuration.”

I must be even denser. How is your claim different from saying “The DNA is not reproducing copies of itself. It is merely catalysing a collection of existing nucleotides to bond in the same order as the DNA’s sequence.”

I.e., sequence and structure are both informatic objects. DNA has no power by itself to create the nucleotides whose assembly it guides. These are synthesized elsewhere. In both cases, only the pattern is replicated, but in both cases it seems fair to me to call it a process of replication.

I grant that the prion mechanism may not be as robust a form of information reproduction as DNA copying (I’m also not saying it isn’t; I don’t know) but I don’t see the obvious distinction. In both cases, we are talking about reproduction of a pattern on a substrate. Likewise, if I use a pencil to plagiarize your writing, I’m merely catalysing some graphite to the same configuration rather than sending your written letters into some kind of magic doubling machine.

What kind of reproduction is there other than the recreation of a pattern on previously existing substrate?

Comment #52421

Posted by Steve S on October 17, 2005 5:59 PM (e)

Comment #52413

Posted by Russell on October 17, 2005 03:25 PM (e) (s)

By the way, there’s a suspicious cluster of CJ disease right now in Idaho

A biostatistics professor friend at NCSU told me that BSE has occured several times in the US already, but it’s been hushed. FWIW.

Comment #52422

Posted by Ron Okimoto on October 17, 2005 6:02 PM (e)

They have some rodent that have PrP knockouts and they can’t get the prion disease. They are talking about making transgenic knock out cattle. There doesn’t seem to be anything very wrong with the knockout rodents, and it probably wouldn’t matter if we made cattle any more brain damaged. I remember the Suzuki nature show where he had cattle on and the narration went something like “fed to stupifaction” with a close up of cattle in a feed lot.

I’d eat PrP knockout transgenic cattle, it could be a turning point for agriculture and transgenic livestock. I’d want it to be a deletion knockout instead of an insertion knockout for obvious reasons.

Comment #52423

Posted by Jason on October 17, 2005 6:09 PM (e)

Syntax Error: mismatched tag 'url'

Comment #52424

Posted by Jason on October 17, 2005 6:12 PM (e)

PUHLEEEZ don’t do this; it’s the kind of presentation that confuses the ‘lay’ reader and fosters misunderstanding of the evolutionary process.

It’s just this kind of wording that this website:
http://www.creationsafaris.com/crevnews.htm
and others use the fool the unsuspecting reader. The constantly use biolgists’ tendency to “anthropomorhpize” molecular and cellular structures and functions as evidence for divine influence in biology.

Example:

http://creationsafaris.com/crev200510.htm#20051004a

I used the tage correctly but it keeps saying I have a syntax error.

Comment #52431

Posted by sanjait on October 17, 2005 9:34 PM (e)

“What would be selected on in the case that is of primary interest to us, BSE?”

“I’d want it to be a deletion knockout instead of an insertion knockout for obvious reasons.”

I’m not a prion expert (how many are there in the world anyways? very few I’d guess), but the presence of similar prions, with compatible conformation changing abilities in many mammals ie sheep, cows, humans, mice etc., suggests there may be a selective pressure preserving it. I don’t think it is known what the protein involved does, even in the non-prion state, but it wouldn’t be surprising to find that both a) the gene does something, which is how it was selected and conserved, and b) the conformation changing capacity contributes to that function, which is how it was selected and conserved.

Comment #52432

Posted by Tony Warnock on October 17, 2005 10:24 PM (e)

The idea of a random graph (representing entities, sheep, cattle, people, etc.) with connections representing infection routes for prions (and I guess for other things) makes me think of a percolation problem.

As percolation is a eigenvalue problem, perhaps some epidemiological models should show this behavior. Under a certain connectivity threshold, few if any entities would be infected; above that threshold, all would. It’s like dissolving boullion in water, only the surface gets wet; with bigger pores, saturation occurs instantly.

Comment #52435

Posted by RBH on October 17, 2005 11:08 PM (e)

Yup. Percolation on heterogeneous networks as a model for epidemics.:

We consider a spatial model related to bond percolation for the spread of a disease that includes variation in the susceptibility to infection. We work on a lattice with random bond strengths and show that with strong heterogeneity, i.e. a wide range of variation of susceptibility, patchiness in the spread of the epidemic is very likely, and the criterion for epidemic outbreak depends strongly on the heterogeneity. These results are qualitatively different from those of standard models in epidemiology, but correspond to real effects. We suggest that heterogeneity in the epidemic will affect the phylogenetic distance distribution of the disease-causing organisms. We also investigate small world lattices, and show that the effects mentioned above are even stronger.

RBH

Comment #52502

Posted by Matthew Cromer on October 18, 2005 5:47 PM (e)

Yes the Darwinian fundamentalists are quite accomodating when the theory doesn’t contradict their mechanistic dogmas.

However, given evidence that challenges the reductionist mindset, their sense of curiosity suddenly departs.

I don’t see a lot of difference between dogmatic reductionistic materialists who ignore evidence which contradict their dogmas, and dogmatic young-earth creationists who ignore evidence which contradicts their dogmas.

Comment #52507

Posted by sir_toejam on October 18, 2005 6:12 PM (e)

aww matt, your response is so replete with standard creationist buzzwords:

darwinian (fundamentalist)
mechanistic dogma
recuctionist
etc etc

one wonders if you have any original thoughts? ever thought about applying the same terminology to your own “mindset”? those terms are far more applicable there.

especially when it comes to “ignoring evidence”… care to present any actual scientific evidence to support your own dogma??

Comment #52509

Posted by sir_toejam on October 18, 2005 6:17 PM (e)

addendum:

before you repost your supposed “given evidence” link; understand what it is that you propose as “evidence” first. what exactly do you think this link provides as real scientific evidence, and what does this evidence actually support, eh?

i think the big thing you missed there was the actual title of the article you linked to:

“Science is a method, not a position “

indeed. now if you understood what that meant, you would also understand how silly it is to apply your misused buzzwords to scientists in general.

Comment #52515

Posted by 'Rev Dr' Lenny Flank on October 18, 2005 6:36 PM (e)

mechanistic dogmas.

I’m curious — in what way do you think “darwinism” is “mechanistic dogma” that, say, “newtonism” or “faradayism” or “einsteinism” isn’t?

Please be as specific as possible.

Oh, and please feel free to explain to me why “mechananistic dogma” in biology is bad, in your view, but “mechanistic dogma” in, say, weather forecasting is not.

Or do you practice divine weather forecasting as well as divine biology?

Comment #52518

Posted by sir_toejam on October 18, 2005 6:43 PM (e)

there is an einsteinism? is that folks who believe in E=MC2, but don’t believe in quantum menchanics?

Comment #52519

Posted by Andrea Bottaro on October 18, 2005 6:48 PM (e)

I’m curious —- in what way do you think “darwinism” is “mechanistic dogma” that, say, “newtonism” or “faradayism” or “einsteinism” isn’t?

Lenny, Matthew seems to be a fan of Rupert Sheldrake, he of psychic research, ESP, “morphic fields”, etc (and good friend of Sermonti’s, which may be what brought him here). Anyway, I am quite sure Matthew disagrees with “newtonism”, “faradayism” & C juts as much as with “darwinism”.

Comment #52523

Posted by Steve S on October 18, 2005 7:04 PM (e)

Oooo, we’ve got a new one. And this guy believes in Parapsychology. I predict amusement in my future. I guess I’ve got The Sight.

Glad to see some fresh blood around here. As glad I am that David Heddle wandered back to oblivion. Though I’m afraid he’ll be back one day, with a new word, representing a new unknown number, which is supposed to prove everything. It’ll go something like

Heddle: The Specificated Enumeration proves ID!
Us: What is it?
Heddle: Who knows?!
Us: How do you calculate it?
Heddle: Who cares?! 120 Orders of Magnitude!
Us: ugh this again.
Heddle: Krauss mentioned a problem. Are you calling him a liar?
Us: (checks tv guide, sees what else we could be doing…)

Comment #52532

Posted by Matthew Cromer on October 18, 2005 7:27 PM (e)

Actually it’s not Darwinism per se which I am arguing against. After all, Darwin himself believed in Lamarkian inheritance.

Anyway, science is not supposed to be about belief. It is about inquiry. Here is an excerpt from a debate between Rupert Sheldrake and Lewis Wolpert. Ask yourself whether science means making dogmatic statements without even looking at the evidence:

I noticed when the parrot film was showing Lewis wasn’t looking at it… He said “telepathy is just junk, there is no evidence whatsoever for any person, place, or thing to be telepathic.” The filmmakers were surprised that he hadn’t actually asked to see the evidence before he commented on it. I think this is rather like the Cardinal Bellamine and people not wanting to look through Galileo’s telescope. I think we have a level here of just not wanting to know – which is not real science, I’m sorry to have to say it Lewis….So we have a self-reinforcing system here … He doesn’t believe it, most people don’t agree with it, it’s not in the top journals, it’s all junk, it’s all pathological science… The fact is, this is a self-reinforcing system, reinforced by a system of taboos and prejudices which I think are a shame to science. I think that this is an outrage, really, that in the scientific world we have this kind of behavior going on which I think brings discredit on the whole of science… I think one of the things which really disillusions people with science is the feeling that science is not actually about evidence, it’s about dogma.

Comment #52534

Posted by Steve S on October 18, 2005 7:32 PM (e)

Two Galileo references by wackos in one day? That’s unlikely. Oh wait it’s not. Pseudoscientists looooove talking about Galileo.

Comment #52536

Posted by sir_toejam on October 18, 2005 7:49 PM (e)

After all, Darwin himself believed in Lamarkian inheritance.

i’m confused as to why this makes you not argue against “darwinism”?

could you possibly seperate the theory from the man, or are you like all the other nutters that come here and presume to know everything about evolutionary theory because you read some clips (or even comments about) the Origin of Species?

get a clue, then come back and you wil be more entertaining.

Comment #52539

Posted by Matthew Cromer on October 18, 2005 7:57 PM (e)

I’m curious —- in what way do you think “darwinism” is “mechanistic dogma” that, say, “newtonism” or “faradayism” or “einsteinism” isn’t?

Please be as specific as possible.

Oh, and please feel free to explain to me why “mechananistic dogma” in biology is bad, in your view, but “mechanistic dogma” in, say, weather forecasting is not.

Or do you practice divine weather forecasting as well as divine biology?

Well if by “Darwinism” you mean that the history of evolution is explained by natural selection of random mutations, I would say that it is a remarkably weak theory with extraordinary little evidence, believed for more-or-less religious reasons. Newton and Faraday’s theories are good approximations, although a century or more out of date as theories of physics. But I’m not surprised to see them trumpeted at a reductionist biology site, as that is the mindset of billiard-ball atomism which pervades so many biologists today, instead of the universe of ubiquitous connection shown by quantum mechanics.

Sometimes the evidence requires science to expand its horizons. And sometimes scientists fail to rise to the occasion, even when the evidence comes from their own experiments. I think Robin Hanson has sketched out what is wrong with institutionalized science quite nicely. Anthony Freeman has some very cogent points too.

Comment #52541

Posted by Matthew Cromer on October 18, 2005 8:07 PM (e)

Two Galileo references by wackos in one day? That’s unlikely. Oh wait it’s not. Pseudoscientists looooove talking about Galileo.

No, real “pseudo”-scientists argue by mockery instead of examining and addressing the evidence. I’m sorry, calling people names is not science, it’s religious dogmatism. Science is a method of inquiry, not a dogmatic position on what is real.

Comment #52542

Posted by sir_toejam on October 18, 2005 8:12 PM (e)

I would say that it is a remarkably weak theory with extraordinary little evidence

unless you want to be painted as a complete moron by BOTH sides in this debate, i highly suggest you actually peruse the literature before you make statements like that.

you can start here, just to scratch the surface:

http://www.talkorigins.org/

from there you can access the some of the primary literature which provides mountains of evidence in support of current evolutionary theory. This evidence is not discounted by the supposed “heads” of the ID movement, they merely interpret it differently (and incorrectly, of course).

once you get to the point where you at least understand the evidence that DOES exist, you can then move on to the stage where you misinterpret it; at that point your arguments would at least be on a par with the current ID movement’s leaders.

creationist buzzwords used by Matt in his most recent post:

random mutations
remarkably weak theory
little evidence
believed for religious reasons (use that mirror again, matt)
reductionist
mindset
atomism

Matt also ascribes things to “quantum mechanics” that obviously have no bearing on the application or theory of.

doesn’t understand why we brought up newtonian mechanics to begin with (thinks we are “trumpeting” newtonian theory *snort*)

thinks that science has failed because it doesn’t support his mythos.

sorry matt, you really need to rethink your whole understanding of what science is, and how it is done. ask lenny nicely and he might post his list of what constitutes an actual scientific theory, and what is involved in testing it. or you could actually do some research yourself on the topic, and actually learn something (tho i seriously doubt you are interested in learning anything).

bye now.

Comment #52578

Posted by Alan on October 19, 2005 2:19 AM (e)

Re previous comment.

I guess I’m thinking of variant CJD. The prion deposits form irreversibly and the infected person dies. Can this same process be used for information storage and does that mean the process is then reversible? Presumably this would then be an avenue to explore for producing a possible cure for CJD.

Comment #52579

Posted by Alan on October 19, 2005 2:25 AM (e)

Sorry seem to have messed up link. Should be this comment.

Comment #52582

Posted by DrFrank on October 19, 2005 6:46 AM (e)

Ah, how I love the badly uncontrolled experiments of parapsychologists such as Sheldrake. I’ll use the staring experiment as an example as I’ve read about it (and its flaws) before.

The staring experiments to do with determining through telepathy/mystic force/vibrations/the will of God/my pet dog whether someone is staring at your back or not. The paper linked to on Matthew’s site contains great lines such as (paraphrasing):

The probability of observing the results by chance was 1 in 10^-376. However, since the test was unsupervised (it was computer automated), people might have been cheating.

Yup, so the results of that experiment mean exactly nothing.

Also, Sheldrake also used sequences with a predictable pattern, and also gave feedback as to whether people were right or wrong with each answer. With exactly 5 staring and 5 non-staring conditions per set in most cases, this was a significant amount of information.

See http://www.csicop.org/si/2000-09/staring.html for more info.

Whenever proper scientific controls are applied, the phenomenon stops, which is why psi phenomena are disregarded by real scientists. If you don’t believe this is the case, you can always apply for Randi’s $1000000 prize at http://www.randi.org, and make yourself some quick cash. Or, in fact, perform any of the psi phenomena you describe on your page. If you don’t have the ‘gift’, then find someone who does and persuade them to do it instead.

If psi phenomena were real, it would be one of the most incredible areas of scientific exploration humanity has ever seen, and every scientist would be clamouring for grants to investigate it. Unfortunately, they aren’t, so they’re not.

Comment #52583

Posted by DrFrank on October 19, 2005 6:48 AM (e)

Wow, three “also”s in one sentence. Please mentally remove the last two lol.

Why is it only after I post that I notice these things? Damn you FSM! *shakes fist*

Comment #52584

Posted by Alan on October 19, 2005 6:55 AM (e)

PaulC wrote:

What kind of reproduction is there other than the recreation of a pattern on previously existing substrate?

So how is information stored and retrieved in a system using prion proteins?

Comment #52588

Posted by 'Rev Dr' Lenny Flank on October 19, 2005 7:06 AM (e)

Well if by “Darwinism” you mean that the history of evolution is explained by natural selection of random mutations, I would say that it is a remarkably weak theory with extraordinary little evidence, believed for more-or-less religious reasons.

I see. And we should care what you say because …… . ?

Comment #52589

Posted by 'Rev Dr' Lenny Flank on October 19, 2005 7:08 AM (e)

I’m sorry, calling people names is not science, it’s religious dogmatism.

Science deals with evidence. Got any? Let’s see it.

Got nothing but quotes from nutters? Then go away, and come back when you have evidence.

Comment #52592

Posted by Matthew Cromer on October 19, 2005 7:56 AM (e)

Whenever proper scientific controls are applied, the phenomenon stops, which is why psi phenomena are disregarded by real scientists.

If you would bother to read the links I posted, you would see that this assertion has been falsified.

This one just for starters.

Science deals with evidence. Got any? Let’s see it.

I’ve already posted lots of evidence. Go read it.

Comment #52593

Posted by Matthew Cromer on October 19, 2005 8:01 AM (e)

Ah, how I love the badly uncontrolled experiments of parapsychologists such as Sheldrake. I’ll use the staring experiment as an example as I’ve read about it (and its flaws) before.

The staring experiments to do with determining through telepathy/mystic force/vibrations/the will of God/my pet dog whether someone is staring at your back or not. The paper linked to on Matthew’s site contains great lines such as (paraphrasing):

The probability of observing the results by chance was 1 in 10^-376. However, since the test was unsupervised (it was computer automated), people might have been cheating.

You might as well claim that intro chemistry experiments are worthless because they are poorly controlled.
Obviously the point of this particular trial is education of the people who perform it in a science museum. Sheldrake has done plenty of well-controlled trials, and this phenomena has been replicated by many other researchers, including skeptics.

Comment #52595

Posted by DrFrank on October 19, 2005 8:17 AM (e)

Well, for a start, here’s Richard Wiseman, the skeptic quoted in your article, explaining why Sheldrake is talking rubbish, and why:

http://www.findarticles.com/p/articles/mi_m2843/is_2_27/ai_98252953

In each study we examined the claim that the dog’s first visit to a certain door in his owner’s house would coincide with his owner setting off to return home from a remote location. On each occasion the dog failed to accurately signal his owner’s return

That was the test. It failed. Sheldrake then reinterpreted the data and objective of the experiment as necessary until, hey presto, it matched his pre-designated conclusions. Wiseman also explains this result without need for magic.

What a wonderful example of confirmation bias.

So again, with the addition of proper controls and a well-defined objective, no effect was observed.

I’ve already read much of the stuff that you’ve posted, as I find pseudoscience entertaining, and I’ve also read the detailed rebuttals of why the studies were methodologically flawed, and also the counter-arguments and so on. You appear to still be at the first step of this process.

You may also want to look up Project Alpha as the ultimate example of what can go wrong with biased investigators in Psi experiments. http://skepdic.com/projectalpha.html

Comment #52596

Posted by ben on October 19, 2005 8:19 AM (e)

Wow. “Lots of evidence.” Every single link you’ve provided is from the same blog. Overwhelming.

“Now that’s what I call believable testimony!”
–Lionel Hutz, Atty.

Comment #52604

Posted by DrFrank on October 19, 2005 10:00 AM (e)

You might as well claim that intro chemistry experiments are worthless because they are poorly controlled
Chemistry itself does not cheat and cannot be biased (no jokes about semiconductors, please :P). The experimenter could only a) perform the experiment incorrectly b) interpret the findings incorrectly or c) commit outright fraud. Other researchers would attempt to replicate their results, particularly if the results ran against current knowledge about chemistry and, if they could not be replicated, the work would be discarded.

When you’re dealing with people, as with all psychology and psi experiments, strict double-blind randomised control trials are essential, along with clearly defined objectives. Performing post-hoc analysis to find variables which correlate is unacceptable, especially when the dog’s behaviour has a much more mundane and plausible explanation. Plus, of course, most correlations are completely meaningless, apart from that one about Global warming and pirates.

Calling your page “Skeptic Proves Psi”, when Wiseman’s conclusions were completely the opposite, is more than a little dubious. Check Richard Wiseman’s page at the University of Hertfordshire, confirming the previous link about his evaluation of Sheldrake’s work http://www.psy.herts.ac.uk/wiseman/research/psychics.html

Psi is a lot like Design (to try and bring this marginally back on topic): both are eliminative arguments, and can only be accepted when every other naturalistic explanation has been removed. If incredibly strict controls have not been added to remove every possibility of the normal senses being used and/or cheating, then the experiment is worthless. Psi researchers such as Sheldrake immediately think “Hey, they’re psychic!” rather than “Oops, maybe my experiment was methodologically flawed”.

Remember the adage “Extraordinary claims require extraordinary evidence”.

Comment #52614

Posted by Matthew Cromer on October 19, 2005 11:09 AM (e)

That was the test. It failed. Sheldrake then reinterpreted the data and objective of the experiment as necessary until, hey presto, it matched his pre-designated conclusions. Wiseman also explains this result without need for magic.

What a wonderful example of confirmation bias.

So again, with the addition of proper controls and a well-defined objective, no effect was observed.

It wasn’t a “test”. It was an experiment. Science is about conducting experiments, not conducting arbitrary “tests” based on media claims which you then get to claim as failures while ignoring the data. Wiseman was completely familiar with Sheldrake’s claims for the data which was not “post-hoc” at all, he used Sheldrake’s equipment and was recording data at Sheldrake’s invitation. Go do some reading.

Wiseman’s data replicates Sheldrake’s. Go look at it again. The pattern is absolutely clear. This is not “post-hoc”, this is the data which Sheldrake showed Wiseman before Wiseman conducted his “tests”. Bottom line, end of story. That’s what science is about – measuring and analyzing the data, and the data is absolutely clear. Wiseman is acting as a media PR hack, not a scientist in this case.

Do you want to be a scientist, or a dogmatist?

Comment #52615

Posted by Matthew Cromer on October 19, 2005 11:11 AM (e)

Wow. “Lots of evidence.” Every single link you’ve provided is from the same blog. Overwhelming.

In all of my blog entries there are these funny little things called “hyperlinks”. Try clicking them sometime. You might learn something!

Comment #52616

Posted by Flint on October 19, 2005 11:38 AM (e)

Sigh. Yeah, the Will To Believe is as strong among scientists as among quacks. Confirmation bias isn’t by any means the realm of only the wingnuts. So the question is, if an experiment confirms our bias, how should we respond? Those who are instantly suspicious and attempt to reconstruct their experiments so that the bias is not the default, and/or requires pretty obviously lousy technique to generate, are following the precepts of science. Those who find non-obvious ways that their results confirm their bias (and then trumpet and glory in these “results”) tend to fall into another category.

It’s probably useful at the point to observe that the casino/gaming industry isn’t the least bit worried by any of these results. They have very strict controls on their methods, and look with ferocious intensity at ANY pattern of results outside the boundaries of random chance. Nor is the stock market affected, nor the lotteries, etc. etc. etc. And compared to the rewards from any of these sources, Randi’s million is chicken feed.

One thing typical of the Will To Believe, however: Those people are very very careful not to look at, like, places where their Beliefs would make a major difference. Yet another illustration of confirmation bias, of course.

Comment #52641

Posted by DrFrank on October 19, 2005 1:54 PM (e)

It wasn’t a “test”. It was an experiment. Science is about conducting experiments, not conducting arbitrary “tests”
And the difference between an experiment and a controlled test is…?

In all of my blog entries there are these funny little things called “hyperlinks”. Try clicking them sometime. You might learn something!
Yes, and a lot of your links are from Sheldrake and Radin. Marks for balanced reading, there.

Given that Pamela Smart was co-credited on the paper, and it was her dog Jaytee, then I am fairly suspicious about the results. The stats presented do appear positive, but this is only one dog and one owner, and both Smart and Sheldrake has a vested interest in obtaining positive results: Smart because it is her dog, and Sheldrake to prop up his “morphic resonance” hypothesis. I believe that if any cheating has gone on, though, then it lies with Smart and not Sheldrake. This is based on the fact that Smart has subsequently disallowed testing by the JREF for the $1000000 (and Sheldrake agreed to be involved in the project), which is a shame because that would gain a lot of credibility, not to mention cash. After doing this twice before for free, I’d certainly be open to do it again for a truckload of money, wouldn’t you?

In short, I believe that more testing is required on different people/animals to provide any passable evidence for this claim.

Comment #52642

Posted by Matthew Cromer on October 19, 2005 1:55 PM (e)

One thing typical of the Will To Believe, however: Those people are very very careful not to look at, like, places where their Beliefs would make a major difference. Yet another illustration of confirmation bias, of course.

Of course if you were correct then Radin’s studies of lottery results and casino payouts varying with GMF wouldn’t exist.

It is those with a will to disbelieve who keep running away from the evidence. And that, of course, is not science, it is dogma, it is religion, it is ignorance.

Comment #52646

Posted by Matthew Cromer on October 19, 2005 2:00 PM (e)

Given that Pamela Smart was co-credited on the paper, and it was her dog Jaytee, then I am fairly suspicious about the results. The stats presented do appear positive, but this is only one dog and one owner, and both Smart and Sheldrake has a vested interest in obtaining positive results: Smart because it is her dog, and Sheldrake to prop up his “morphic resonance” hypothesis.

Wiseman had no vested interest in obtaining positive results – but he replicated Sheldrake’s data.

Sheldrake has studied a number of return-anticipating dogs, but obviously focused his most rigorous trials on the best performers. He also has a lot of other work on his plate, to say the least. Here’s another videotaped dog study.

Comment #52648

Posted by Matthew Cromer on October 19, 2005 2:02 PM (e)

BTW Pam Smart is now Sheldrake’s research assistant and has been for 10 years or so, AFAIK. They are both extremely helpful and friendly via email.

Comment #52649

Posted by sir_toejam on October 19, 2005 2:07 PM (e)

bah. matt is a “true believer”. you will never be able to convince him that his beliefs are at best based on pseudoscience. Unless you are telepathic, of course ;)

matt, you won’t win any converts here, because most folks here subscribe to the scientific method. something you obviously fail to understand. why do you bother? If you can’t accept how science works, don’t. we won’t force you to accept it. just realize that you don’t and move on.

Comment #52652

Posted by sir_toejam on October 19, 2005 2:15 PM (e)

personally, i was finding the debate between prions as poisons vs. replicating vectors much more interesting. could we get back to that?

unless matt can figure out some psi spin to prions, of course…

Comment #52662

Posted by DrFrank on October 19, 2005 2:36 PM (e)

it is dogma, it is religion, it is ignorance.

And this coming from someone who says

Well if by “Darwinism” you mean that the history of evolution is explained by natural selection of random mutations, I would say that it is a remarkably weak theory with extraordinary little evidence, believed for more-or-less religious reasons

I’m not sure why I’ve even bothered to discuss scientific evidence with someone who’d come out with something like that. I guess the flu I have is affecting my judgement.

Why not present your evidence against evolution or point out the big holes in the theory for us all, so that we may all be enlightened?

Comment #52664

Posted by Flint on October 19, 2005 2:42 PM (e)

it is dogma, it is religion, it is ignorance.

And here also, I’ll point out that casinos take this religious dogma straight to the bank every day. Their returns match their calculations within a tiny fraction of a percent, week in and week out. But matthew has a book written for the explicit purpose of separating Psi True Believers from their money, wherein the author says casinos don’t realize that psi is working against them, (and forget the actual returns). I wonder if this guy Radin can name a single individual ever discouraged from gambling because of psi ability? Anyone want to bet?

Comment #52673

Posted by CJ O'Brien on October 19, 2005 3:17 PM (e)

I’m pretty sure, every time I gamble, that I’ll lose money. I’m usually right.

Holy Toledo, I’m psychic!
(RIP Bill King)

Comment #52674

Posted by DrFrank on October 19, 2005 3:17 PM (e)

Looking at the Kane dog case study, I think the major confounding variable was that the owner’s partner was in the house most of the time and could may have subconsciously cued the dog as to when he believed the owner’s arrival was imminent. Animals can certainly pick up subtle physical clues like this, as determined by Clever Hans. They only performed three trials when the partner did not know when she would arrive, and the dog completely failed on one of these.

Also, the amount of time the camera was on for before the owner came home was quite consistent in the graphs in Figure 3, and Kane may well have learnt to use this information.

I’m sure Randi would quite happily also test Kane for this telepathy if his owners did not object (unlike Smart), and hand over the $1000000 if he reproduced such results.

Comment #52685

Posted by Matthew Cromer on October 19, 2005 4:27 PM (e)

Why not present your evidence against evolution or point out the big holes in the theory for us all, so that we may all be enlightened?

You must have a reading comprehension problem. I’m an evolutionist. I just don’t buy that evolutionary history / complexity is explained via blind selection of random mutations.

Dr. Frank, those are good thoughts about Kane. I’d be happy to discuss them at my blog, if you are willing to post them there. I’m done with this thread here, the S/N ratio is too high from people who think mockery and insult are a kind of scientific evidence. People who blather about the scientific method and “true believers” but can’t be bothered to actually read studies which disagree with their authority figures. I would be more than happy to discuss JayTee, Kane, Randi’s 1 million dollar prize etc. on my blog. I even post well-written articles by skeptics there.

Comment #52694

Posted by Flint on October 19, 2005 4:52 PM (e)

I’m an evolutionist. I just don’t buy that evolutionary history / complexity is explained via blind selection of random mutations.

This sounds a bit suspicious. “Blind” selection? Uh, isn’t that a contradiction in terms? I submit that the ONLY way you could write such a thing without it engaging your mental gears at all, is if it were already memorized for some reason. I wonder what that reason might be. But not real hard.

Comment #52697

Posted by sir_toejam on October 19, 2005 5:05 PM (e)

You must have a reading comprehension problem. I’m an evolutionist. I just don’t buy that evolutionary history / complexity is explained via blind selection of random mutations.

no we read just fine. it’s you who have a comprehension problem. if you actually understood the theory of evolution, rather than just spouting nonsense, or if you bothered to actually go and read about it at the talk.orgins site i recommended to you, you would know that:

-selection is far from a “random” process
-random mutations are only one force driving genetic diversity

i warned you folks here would think you a moron if you proceeded to continue exposing your lack of understanding of the topic so readily. Now go do some reading, moron.

go peddle your wares elsewhere.

Comment #52698

Posted by DrFrank on October 19, 2005 5:18 PM (e)

You must have a reading comprehension problem. I’m an evolutionist. I just don’t buy that evolutionary history / complexity is explained via blind selection of random mutations.

I’m guessing from your support of Sheldrake that you’re a supporter of formative causation. If so, the arguments I’ve read as to the need to posit some kind of supernatural field to govern the growth of a cell into a large multicellular creature such as a human appear to be severely lacking.

Comment #52722

Posted by 'Rev Dr' Lenny Flank on October 19, 2005 6:25 PM (e)

Science deals with evidence. Got any? Let’s see it.

I’ve already posted lots of evidence. Go read it.

BWA HA HA HA !!!!!!!!!!!!!!!!!!!!!!

Hey, where do the space aliens fit into all this?

(snicker) (giggle)

Comment #52723

Posted by 'Rev Dr' Lenny Flank on October 19, 2005 6:28 PM (e)

I’m an evolutionist. I just don’t buy that evolutionary history complexity is explained via blind selection of random mutations.

Wait, let me guess —- the space aliens diddit. Right?

Or does our cosmic aura play some role?

(snicker) (giggle)

Hey, I notice that none of the IDers here are piping up in support of our new friend. Maybe their Big Tent, uh, isn’t THAT big.

BWA HA HA HA !!!!!!!!!!!!!!!!!!!

Comment #52807

Posted by Alan on October 20, 2005 2:13 AM (e)

Sir T wrote:

personally, i was finding the debate between prions as poisons vs. replicating vectors much more interesting. could we get back to that?

Seconded. “Debating” with cranks is a waste of time. I was really hoping someone could pick up on the queries in comments #52584, 52578
and 52401.

Comment #52809

Posted by Alan on October 20, 2005 2:57 AM (e)

For instance

PaulC wrote:

How is your claim different from saying “The DNA is not reproducing copies of itself. It is merely catalysing a collection of existing nucleotides to bond in the same order as the DNA’s sequence.

“in the same order” would be the difference to prion folding. Is there a template, sequence ordering, a code based on order, position, quantity, variation in prion structure which incorporates information and how is the information accessed? There seem to be answers when substituting “DNA” for”prion”.

Comment #52815

Posted by sir_toejam on October 20, 2005 4:17 AM (e)

so you would lean towards thinking of prions more like “poisons”, then?

Comment #52821

Posted by SteveF on October 20, 2005 5:48 AM (e)

Speaking about the inflexible Darwinian orthodoxy, a paper in the latest issue of Nature provides yet another perfect example of this.

“Evolutionary biology: Fruitfly genome is not junk, p1106

A comparison of two fruitfly genomes shows that much of their non-coding DNA is controlled by either negative or positive selection, dealing a double blow to the neutral theory of molecular evolution.

Alexey S. Kondrashov”

I can see the ID crowd getting all sweaty and excited over this paper.

Comment #52857

Posted by Henry J on October 20, 2005 11:26 AM (e)

Re “shows that much of their non-coding DNA is controlled by either negative or positive selection”

Why on earth would anybody think that would conflict with the ToE? ToE didn’t predict that there’d be a lot of unused DNA, afaik.

Henry

Comment #52866

Posted by SteveF on October 20, 2005 12:24 PM (e)

“Why on earth would anybody think that would conflict with the ToE? ToE didn’t predict that there’d be a lot of unused DNA, afaik”

Apparently its a ‘prediction’ of ID, that that ‘junk’ DNA isn’t junk after all. Not really sure why ID makes this prediction (surely an intelligent designer can make as much or as little junk as he/she/it wants).

Comment #52871

Posted by Alan on October 20, 2005 12:58 PM (e)

so you would lean towards thinking of prions more like “poisons”, then?

Well, infectious agents, certainly in the case of CJD. No, Sir T, I was interested in the proposition that prions could be connected with long term memory in sea slugs, as it seemed to suggest a possible cure for CJD. I assumed this implied reversibility of the folding cascade. On re-reading I suspect I am wrong or at least premature. I think the process of long-term memory formation postulated just involves reinforcement of the relevant nerve pathways with prion deposits.

BTW my wife is rationing my access to the Internet at the moment, so posts can be a bit erratic.

Comment #52881

Posted by PaulC on October 20, 2005 1:53 PM (e)

Is there a template, sequence ordering, a code based on order, position, quantity, variation in prion structure which incorporates information and how is the information accessed?

Sure. A prion protein stores at least one bit of information. It can either be in the normal conformation or the prion conformation. This bit is encoded by a particular set of assignments to torsion around some of the bonds in the protein chain. When the prion replicates, that bit is read from the prion and written into the normal protein. So the prion implements a sort of self-actuating write-once 1-bit memory. I don’t think it’s known whether it can store more than 1 bit or whether the prion conformation is reversible. But it’s not obvious to me why you would rule out the possibility of additional storage capacity in protein structures. There are many degrees of freedom, and multiple local energy minima. So prions might be a one-trick pony, or they could be an example of a more robust informatic mechanism not yet understood (I’ll leave it to biologists to place odds.)

It’s true that the prion does not store any information about how to build the 1-bit memory. But a DNA sequence does not directly encode the information about the molecular structure of nucleotides either, and only functions in an environment that is already rich in some of the components of these. All I’m saying is that the question of replication in DNA vs. prions strikes me as a matter of degree rather than kind. But I can also see why you might prefer to view it differently.

Actually prions strike me as an awful lot like Kurt Vonnegut’s fictious “Ice-9”, a self-catalyzing room-temperature solid form of water. It is replication in the same sense as crystallization. That makes it somewhat limited, but nothing like a convention poison, which is not self-catalyzing and can effectively be diluted.

Comment #52909

Posted by sir_toejam on October 20, 2005 4:19 PM (e)

I can see the ID crowd getting all sweaty and excited over this paper.

ewwww. now i have to go scrub my eyeballs.

Comment #52912

Posted by sir_toejam on October 20, 2005 4:25 PM (e)

as it seemed to suggest a possible cure for CJD. I assumed this implied reversibility of the folding cascade

interesting. However, I’m not sure that the reverse process would be anything like the forward one. OTOH, research using prions might actually lead to catalyzing mechanisms that would get you there.

wouldn’t be the first time a poison has led to a cure.

indeed, most interesting.

Comment #52915

Posted by Henry J on October 20, 2005 4:32 PM (e)

Re “Why on earth would anybody think that would conflict with the ToE? ToE didn’t predict that there’d be a lot of unused DNA, afaik”

Re “Apparently its a ‘prediction’ of ID, that that ‘junk’ DNA isn’t junk after all. Not really sure why ID makes this prediction (surely an intelligent designer can make as much or as little junk as he/she/it wants).”

I suppose it’s logical that a deliberate design would avoid unused pieces, since they’d take energy to produce and maintain. Then again, the ToE would also predict that, wouldn’t it? Or at least suggest that it’s likely?

Though the more interesting question would be what that other 90 something % does for the species. Does it serve as raw material for future evolution? Does it serve as spacing between coding genes to avoid congestion of the chemicals trying to read them? Does the length of a stretch of “junk” dna have some affect on timing of something? Are the I.D. people asking any of these questions? (I guess that last one was rhetorical. :) )

Henry

Comment #52926

Posted by sir_toejam on October 20, 2005 5:03 PM (e)

“Though the more interesting question would be what that other 90 something % does for the species individual”

Comment #52948

Posted by 'Rev Dr' Lenny Flank on October 20, 2005 6:19 PM (e)

I have a question; if a prion induces a mis-folded protein that matches the prion, and somewhere down the line a misfolded protein is induced that is DIFFERENT than the preceding ones, does the next one continue the ORIGINAL mis-folding, or the new one?

I.e., do prions mutate and then inherit those mutations?

Comment #52951

Posted by sir_toejam on October 20, 2005 6:27 PM (e)

@Henry

btw, it’s not as if nobody is researching the function of non-coding DNA; it’s not my field of expertise, but i can recall reading several studies in the late 80’s early 90’s even, so I’m sure there is a plethora of articles that could be easily accessed at the local university library, should you be so inclined. I’m sure a start could even be made using google scholar, at least to get abstracts.

let us know if you run accross anything of particular interest. I can only wish Blast could be as productive and actually check out that kind of literature himself. but that would be asking him to learn something, which is like asking a rock to speak on command.

Comment #52952

Posted by sir_toejam on October 20, 2005 6:38 PM (e)

@lenny:

hmm, that seems a good question to me as well. that would depend on whether the new configuration could actually induce structure deformation in and of itself; to catalyze folding to begin with would require a very specific structure, so modifications would likely stop the reaction. However, it would at least seem theoretically possible, even if very unlikely to occur. Hopefully Andrea would know if any studies have indicated whether prion modified proteins have been recorded to spontaneously change, and then whether any cascade reactions have occured from there.

it’s such a new area of study, i wouldn’t be surprised if that has not been recorded yet.

OTOH, the paranoiac in me starts to think of the potential for prions as biological weapons and that would be the first area of research i would start to play with: just how much can a prion be altered and still catalyze folding, and would new shapes produce even more lethal cascade reactions.

*sigh*

Comment #52955

Posted by Steviepinhead on October 20, 2005 6:45 PM (e)

I can only wish Blast could be as productive and actually check out that kind of literature himself. but that would be asking him to learn something, which is like asking a rock to speak on command.

sir_toejam, please, don’t insult the rocks! I’m sure quite a few rocks are more eloquent and articulate than Blast, even if they are the archetypal strong silent types and do generally tend towards the taciturn end of the expressive spectrum.

Besides, I’ve got to climb on those rocks at times, and I really can’t afford for them to get POed at the PTers!

Comment #52956

Posted by Steviepinhead on October 20, 2005 6:48 PM (e)

Hmmm, I guess the technically-correct abbreviation would be PedO

But that looks pretty strange.

Comment #52958

Posted by sir_toejam on October 20, 2005 7:01 PM (e)

my apologies to geological formations everywhere and in every form.

Comment #52959

Posted by CJ O'Brien on October 20, 2005 7:01 PM (e)

Nah. PedO is PedAntic.

Comment #52973

Posted by 'Rev Dr' Lenny Flank on October 20, 2005 8:34 PM (e)

OTOH, the paranoiac in me starts to think of the potential for prions as biological weapons and that would be the first area of research i would start to play with: just how much can a prion be altered and still catalyze folding, and would new shapes produce even more lethal cascade reactions.

*sigh*

As I mentioned in another thread, I do know a few things about the US’s biowarfare “defense” research. Although someone made light of it, it should scare the living crap out of you.

Comment #53011

Posted by Alan on October 21, 2005 2:08 AM (e)

One of the proposed vectors for transfer of CJD from cattle to humans at the height of the BSE epidemic in the UK was Hamburgers. Spiked hamburgers might work as a BW, but you couldn’t get too many in a nosecone. “Incubation” time being so long is also a drawback.

Re prions and memory. With DNA all the machinery for copying, replicating etc. is there. The catalyzing and crystal-forming analogy seems to describe prion “behaviour” well. Is there variation in amino-acid sequence of prion proteins? If so there could be a way of storing information. But you would need a template and a read-write system. Encoding info. in protein sequences which can then be replicated doesn’t happen elsewhere in biological systems, AFAIK. As there is only one conformation for the folded prion, I doubt there is much scope there.

BW, Don’t you just hate analogies, especially those involving Mt. Rushmore or mousetraps?

Comment #53039

Posted by Henry J on October 21, 2005 10:43 AM (e)

Found this article: UCSD Study Shows ‘Junk’ DNA Has Evolutionary Importance . Funny (serendipitous?) that this article happened to come out just as the subject was being discussed here. :)

But, it doesn’t get into what the “junk” dna does, just the fact that it seems to be preserved from some percentage of the possible mutations - which implies selection for some function but doesn’t name the function. The article implies that the specific function isn’t known yet. (Or at least not by the author of said article?)

Henry

Comment #53047

Posted by Alan on October 21, 2005 12:20 PM (e)

It’s a shame it got called junk DNA in the first place.

Comment #53048

Posted by Alan on October 21, 2005 12:20 PM (e)

It’s a shame it got called junk DNA in the first place.