The Discovery Institute has of course picked up Michael Behe’s new paper in Quarterly Review of Biology, and it’s distorted summarized by DI bigwig Casey Luskin here. As I predicted, the IDers completely ignore the limitations of this paper (see my analyses here and here), and assert, wrongly, that Behe has made a powerful statement about evolution in nature.
This distortion is hardly news, of course—I’m completely confident that Behe not only expected it, but approves of it—but I feel compelled to highlight it once again. Luskin’s three distortions, which correspond to the three caveats attached to Behe’s results:
1. Luskin doesn’t mention that Behe’s analysis concentrated only on short-term laboratory studies of adaptation in bacteria and viruses.
2. Luskin also doesn’t mention that these experiments deliberately excluded an important way that bacteria and viruses gain new genetic elements in nature: through horizontal uptake of DNA from other organisms. This kind of uptake was prohibited by the design of the experiments.
3. Luskin implies that Behe’s conclusions extend to all species, including eukaryotes, even though we know that members of this group (and even some bacteria) can gain new genetic elements and information via gene duplication and divergence. And we know that this has happened repeatedly and pervasively in the course of evolution.
Luskin’s intent is clear—to claim that Behe has supposedly shown a profound problem with the theory of evolution and natural selection: it cannot explain the gain of new genetic elements in evolution. There must therefore most be another source of these new elements. Ergo Jesus. Behe did not show this, and Luskin knows it.
Some Luskin quotes from the piece, generalizing from short-term lab experiments on microbes to evolution as a whole in nature:
Behe doesn’t claim that gain-of-function mutations will never occur, but the clear implication is that neo-Darwinists cannot forever rely on examples of loss or modification-of-FCT mutations to explain molecular evolution. At some point, there must be gain of function. But if loss-of-function mutations are so much more common than gain-of-function mutations that the odds of a pathway following a multiple mutation pathway toward the construction of a new FCT before encountering a local adaptive peak that “breaks or blunts” the FCT may be prohibitively small. . .
. . . If Behe’s article is correct, then molecular evolution, in the world of real biology, faces a similar problem. Remember that Behe found that “the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.” If loss/modification-of-FCT adaptations are 100-1000 times more likely than gain-of-FCT adaptations, then logic dictates that eventually an evolving type of organism will run out of FCTs to lose/modify.
In short, the logical outcome of Behe’s finding is that some process other than natural selection and random mutation* must be generating new FCTs. If Darwinian evolution is at work, it tends to remove FCTs much faster than it creates them — something else must be generating the information for new FCTs.
The evidence cited by Behe does not paint a hopeful state of affairs for Darwinian proponents of molecular evolution.
So typical of these clowns to ignore the insuperable problems with extending Behe’s limited conclusions to evolution as a whole. But I’m absolutely sure that Behe intended his paper to be distorted in this way.
This is only the beginning of the ID distortions to come. I don’t plan on writing more about this, but feel free to post further ID shenanigans in the comments.
_________
*[He means Jesus]
Jesus has now been reduced to “The Unfalsifiable FCT Generator.”
This is quite a demotion in cosmic tenure.
This entire thing is merely the the pseudo-biologist’s take on Dumbski’s “information” hypothesis.
I can’t tell you how many times a creatard has said to me “information cannot be gained, only lost” in biological systems.
Behe is merely jumping on the bandwagon.
I expect he’ll deny common descent next — something he hasn’t done in the past.
“If loss/modification-of-FCT adaptations are 100-1000 times more likely than gain-of-FCT adaptations, then logic dictates that eventually an evolving type of organism will run out of FCTs to lose/modify.”
Luskin completely ignores natural selection. Why even bother with this guy?
Luskin has shown up in these comment threads before. Casey: your “summary” shows what happens when biology comes from a lawyer. I’d say more, but I have a manuscript on deadline so I’ll leave further flea swatting to someone else.
Jerry, can you point to experimental studies showing the origin of FCTs in eukaryotes? Examples you gave in previous blogs were post-hoc scenarios — not that there’s anything wrong with that (to quote Seinfeld), but the data were not gained by watching, say, populations of yeast in real time.
I ask because I’m working on an article explaining why Mike Behe focused on experimental data in the QRB paper, and I want to make sure I haven’t missed any such studies using eukaryotes.
Thanks!
Paul,
You know very well that nobody has done these types of experiments in eukaryotes, although it’s a great idea, especially now that we can sequence genomes. But what, exactly, is wrong with post-hoc scenarios? You say that there’s “not anything wrong with them,” and since the evidence for the evolution of gene duplication and divergence is so strong, post hoc, are you simply refusing to accept them as evidence even while admitting that kind of evidence is okay?
Actually, since you’re a young-earth creationist, I don’t think you can be trusted to regard any data with scientific objectivity, since you reject the overwhelming evidence that the earth is old.
But the earth didn’t age in a lab before our eyes; therefore, your evidence doesn’t count.
Jerry wrote:
“You say that there’s ‘not anything wrong with them,’ and since the evidence for the evolution of gene duplication and divergence is so strong, post hoc, are you simply refusing to accept them as evidence even while admitting that kind of evidence is okay?”
Dobzhansky famously worried that postulating evolutionary events beyond the horizon of human observability required what he called “a reluctant sign of equality” (1937, 12) between what we’ve seen in real time, and what we’ve inferred about biological history. Post-hoc scenarios typically require one to postulate selective pressures, populations sizes, etc., which may well not have been the case. The chains of inference are thus a lot longer, and more fragile, than what obtains (say) with bacteria growing in a chemostat, where the number of degrees of freedom in the analysis have been reduced significantly.
You know the problems with post-hoc scenarios, Jerry: you’ve written about them here, on occasion, but also in your published work. “Not that there’s anything wrong with them” simply represents a reasonable caution about the shortcomings of adaptive storytelling on the basis of data such as sequence similarity.
Just to be sure: NO experimental studies have been done in eukaryotes on the origin of what Behe calls FCTs?
Paul, doesn’t duplication and divergence fit Behe’s definition of gain-of-function FCTs? By which I’m talking about the eukaryotic example of Antarctic fish gaining anti-freeze proteins from the duplication and mutation of genes that once coded digestive enzymes.
(I know I said I was busy but I am fresh off a discussion thread the last few days where a YEC uses the same “no new information” argument.)
All of the well-studied vertebrate gene clusters (alpha-like globin, beta-like globin, growth hormone, et al.) are also excellent examples of block duplications followed by functional divergence (even if primarily at the level of tissue- or developmental stage-specificity of expression)
Hey Nelson,
Can you cite one example where forensic evidence was collected before a crime? No? How can that be? “Post-hoc scenarios” need one to postulate a lot of things, right? Does that mean forensic science is bunk?
Should we shut down the whole prison system, Nelson?
Forensic science may be an unfortunate choice for the point you are making. Apart from DNA, forensics wasn’t created by scientists, but cobbled together over the years by police investigators. There are all sorts of problems with fingerprint matching, fiber matching, arson investigation and the like. Even DNA, while scientific, is abused statistically (and a defendant is not even legally allowed to challenge the FBI’s statistics or raise the issue in court).
I hope you are actively campaigning for an end to the prison system.
Nope. Just pointing out that forensic ‘science’ isn’t always scientific. I am, however, actively campaigning not to enter the prison system.
truthinjustice.org is one source that contains hundreds of links about the flaws – including the scientific flaws – in our criminal justice system. The sort of folksy heuristics used in arson investigation (fire always burns up, etc.) are especially terrifying.
Has anyone looked at FCT gains in the transformation of normal cells to tumor cells? In the hamster/SV40 system, the first thing that happens is endoreduplication of the entire genome and then chromososme losses, rearrangements, etc. Might be another eukaryotic example.
Post-hoc scenarios typically require one to postulate [TESTABLE] selective pressures, [MEASURABLE] populations sizes, etc.,
indeed.
and this is an OLD issue that has long since been addressed, and many times, and in the field as well as the lab.
problem is, you clowns refuse to acknowledge there has been any work done since the formation of the modern synthesis!
the blind spot you guys wield pretty much covers everything but the eyes in the back of your head.
” … shortcomings of adaptive storytelling.”
Hmmm. I wonder what Paul’s alternative story is that has no shortcomings?
There is nice work on yeasts.
From the Results of Koszul et al. EMBO J 2004:
“Altogether, the growth defect was compensated by the duplication of the remaining gene of the pair”
http://www.nature.com/emboj/journal/v23/n1/full/7600024a.html
And from Gresham et al. PLoS Genet 2008:
“We detected a second class of prevalent structural variation in evolved clones, consisting of gross chromosomal events. Segmental changes in copy number were detected by CGH (…)”
http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000303
A nice review, but not Open Access:
http://www.nature.com/nrg/journal/v11/n7/full/nrg2811.html
There is also some nice work done with Arabidopsis
“Copy Number Variation Shapes Genome Diversity in Arabidopsis Over Immediate Family Generational Scales”
http://gbe.oxfordjournals.org/content/2/441.long
(I think this is open access).
And that is without even looking hard. The techniques for identifying gene duplications have only become widespread within the past few years so the published studies that identify them in an evolutionary context are limited at the moment (most of the studies have been on human genetics or disease predisposition/cancer).
Thanks for the yeast and Arabidopsis references, which I’ve now downloaded.
Paul, if you are really serious about doing a proper article about this for this then you need to go through the literature on copy number variations that have been published over the past five years. Even for the genomics community the rate of variation between generations was surprising. We simply didn’t realize that such a high rate of gene duplications and deletions were happening. It was actually a shock to see it so clearly when we developed the techniques of comparative genomic hybridization. There have even been several cases of variations found between twins!
Paul,
What Jerry said. Ignoring the massive evidence that gene duplication + divergence is the main source of new “information” = one is a traditional, very silly, creationist hack who will be dismissed as a crank and who will deserve it.
Basically what Behe and his fans are doing by ignoring this obvious, long-known, long-the-dominant-explanation-in-standard-textbook-theory, extremely-well-tested explanation for the origin of new “information” is the equivalent of going to Kansas, observing that the Earth looks flat in their arbitrarily selected extremely limited observational domain, and then concluding that the Earth is probably flat, and then petulantly insisting that the world is flat unless someone can show them that the Earth isn’t flat by direct observation, while never allowing observations that involve something broader than the view from the ground in Kansas.
I vote we dub this kind of thing — stubbornly ignoring obviously relevant evidence, and obsessive focus on one very narrow kind of evidence as the only good evidence — as “Behe’s Blinders”.
(All that said, consider:
1. Mainstream theory says gene duplication + modification of a copy is basically the main source of new genes with new functions.
2. Behe reviews many experiments in which adaptive (even better than neutral spread!) gene duplications are observed in very short-term, very-simple experimental situations.
3. Behe reviews many experiments in which genes successively change function (e.g. new substrates, even to human-created xenobiotic compounds not before seen in nature) through point mutations, observations again made even in very short-term, very-simple experimental situations.
4. Behe concludes we should be skeptical of gene duplication + modification as an explanation of new genes.
This is the only appropriate reaction when confronted with that sort of silliness:
http://www.acr0nym.com/gallery2/main.php?g2_view=core.DownloadItem&g2_itemId=1121&g2_serialNumber=1
“Just to be sure: NO experimental studies have been done in eukaryotes on the origin of what Behe calls FCTs?”
Yeah, no, there is a bnch of stuff with yeasts. Especially because of industrial uses with fermentation, ethanol production for biofuels (and drinking) etc. This one is a classic, long-mentioned on e.g. talkorigins…as far as I can tell it even meets the “new coding sequence” requirement as well:
http://www.talkorigins.org/indexcc/CB/CB102.html
==============
Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further. (Brown et al. 1998)
[…]
Brown, C. J., K. M. Todd and R. F. Rosenzweig, 1998. Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Molecular Biology and Evolution 15(8): 931-942.
==============
Behe argues, in his response to Jerry at the EN&V site, that these aren’t short term experiments as such:
http://www.evolutionnews.org/2010/12/the_first_rule_of_adaptive_evo041811.html
He also makes the case that the results may be more widely applicable (by a somewhat specious looking comparison to humans)
But most them were. Many of the experiments are literally:
(a) put out a petri dish with a limiting nutrient or an antibiotic on it
(b) innoculate with a bacterium derived from a clone
(c) wait a few days, come back, and look for any colonies that are growing — these are colonies derived from some single bacterium that had a mutation that enabled growth in the dish
(d) stop experiment
It is obvious (or should be) why this will tend to detect single adaptive mutations, but not combinations or series of them.
There are some long-term experiments, but fewer of them, and they typically involve very uniform, simple conditions, perhaps with one adaptive challenge (IIRC, citrate limitation in Lenski’s experiment) where dispensing of unnecessary bits may well be useful.
It would be nice to see a long-term experiment where one antibiotic is added, resistance develops, then another, then another, etc., until the microbes have adapted to a complex environment with related and unrelated antibiotic compounds. This is starting to be vaguely similar to the tremendously complex chemical environment that would be found in e.g. soil or mud.
Paul, can you point to experimental studies showing the origin of galaxies in galaxy clusters? Examples that are typically given are post-hoc scenarios — not that there’s anything wrong with that (to quote Seinfeld), but the data were not gained by watching, say, populations of galaxy clusters in real time.
How’s that work on Ontogenetic Depth going Paul?
This distortion is hardly news, of course—I’m completely confident that Behe not only expected it, but approves of it—but I feel compelled to highlight it once again.
Hey, no need to explain – you’re performing a service. You’re explaining it to the public; you’re keeping track; you’re supplying the lawyers with notes that will come in handy for the next Dover.
“… not that there’s anything wrong with that.”
I suspect the most productive course of action is asking what Richard Lenski thinks of this paper. Might be worth sending him an email Jerry?
Incidentally, Behe’s paper is out of date and seemingly not particularly comprehensive. The former because research has come out since (presumably) Behe submitted the paper (dunno if they affects his conclusions as I’m not familiar enough with them). Not his fault but a couple of examples:
Burke, M.K. et al. (2010) Genome-wide analysis of a long-term evolution experiment with Drosophila. Nature, 467, 587-590.
Barrick, J. E. et al. (2010) 2010. Escherichia coli rpoB mutants have increased evolvability in proportion to their fitness defects. Molecular Biology and Evolution, 27, 1338-1347.
and the latter because he misses some Lenski research published in recent years. For example:
Barrick, J.E. et al. (2009) Genome evolution and adaptation in a long-term experiment with Escherichia coli. Nature, 461, 1243-1247.
(Behe knows about this paper because he’s blogged about it at his Uncommon Descent site, discussing it along the lines of his latest paper)
Stanek, M. T. et al. (2009) Identification and dynamics of a beneficial mutation in a long-term evolution experiment with Escherichia coli. BMC Evolutionary Biology, 9, 302 doi:10.1186/1471-2148-9-302.
Philippe, N.L. et al. (2009) Evolution of penicillin-binding protein 2 concentration and cell shape during a long-term experiment with Escherichia coli. Journal of Bacteriology, 191, 909-921
this next paper came out in 2008 (certainly before Behe would have submitted) and isn’t included.
Sleight, S.C. et al. (2008) Genetic basis of evolutionary adaptation by Escherichia coli to stressful cycles of freezing, thawing and growth. Genetics, 180, 431-443
and a paper from 2007:
Philippe, N. et al. (2007). Evolution of global regulatory networks during a long-term experiment with Escherichia coli. BioEssays, 29, 846-860.
I could go on but I can’t be bothered. These papers may or may not impact upon Behe’s conclusions, and I haven’t done much more than glance at the abstract so maybe he spells out the reasons for not including these papers, but at face value he looks to have performed a fairly basic literature review. Guess I’ll have to read the paper to see if he explains why.
I searched your first entry, Steve, and it turns out that Burke’s article demonstrates that after 600 generations of inbreeding flies, very little change has taken place. Further, the classic “sweeps” of population genetics did not appear to happen. In the review of Burke’s paper, found on the ICR website, the Barrick paper is also listed.
Looks like Behe didn’t miss much.
I’m sure IDers will respond to accusations of extrapolating Behe’s paper by saying that evilutionists extrapolate fruit fly research all the time and apply their lab-limited conclusions to “bacteria-to-humans” evolution.
Now that we get down to the nitty gritty, the DI has put itself in a bind as stark as if they had to admit to being speaking for YECs and OECs both.
Behe makes claims on gene functionality. Curiously absent from Luskin’s description is what happens in terms of DIs popular information.
We know that selection channels Shannon information from the environment to the genome. (There is even papers on that, IIRC. But this is also Dawkin’s easily derived model.) Now what Behe observes as “loss-of-FCT” mutations will after selection and fixation disappear genomic material, bases, from the used genome and by drift possibly from the genome altogether. This translates to loss of Kolmogorov information (incompressible information) of either kind.
On the other hand we have Dembski’s ‘research’, where he, in ordinary cases uselessly, sorts new Shannon information as environmentally gained and original Kolmogorov information into two bins, one labeled “nature given := useless” and one labeled “god given := useful”. But here the sort _is_ useful, since we notice that a) Shannon information can make ‘useful’ information (“modification-of-function” and “gain-of-FCT”) that keeps or increases (gene duplications!) Kolmogorov information b) Shannon information can destroy Kolmogorov information.
a) is a DI killer – put Behe and Dembski together and derive a DI supported conflict of dogma.
b) is a twist on DI’s usual “can only destroy information” by way of a), first evolution may destroy gained information too, second the sum total may be a gain.
To paraphrase Luskin:
“The evidence cited by Behe does not paint a hopeful state of affairs for Paleyan proponents of information creationism.”
Is this Casey ‘eponymous’ Luskin?
I just got done reading Stephen Jay Gould.I think he makes a lot of sense on-contingency,on punkek,and on ultra darwinian obsession with natural selection.He also is brutally honest about misguided uses of natselec /eugenics by nazis(he is jewish,after all)why do we waste time arguing with these idiots.It seems that we demonstrate a certain thin skinned ness,in letting their arguments bother us.There is thing the creaos say thats right for all the wrong reasons-we werent there during lifes 4 billion year history.We WILL NOT ever know exactly what happened.One things for sure-jebus aint comin back(i mean whats the holdup-things aint fucked up enough now)
This is the DI’s equivalent of the creationist claim that evolution violates the second law of thermodynamics. The inforformation comes from the same place as does all information, physics. Information is physical, like every other real thing:
Creationists like Luskin and Behe try to get away with this nonsense because very few people understand thermodynamics and information theory.
Pension Deficit Disorder is clearly a powerful driver in the evolution of ID as an income generating mechanism.
I work in cancer genetics which means I am constantly confronted witj examples of these types of gain of function mutations. The classic examples are the fusion genes resulting from chromosomal translocations that join exons from two separate genes to produce a new gene with a different function.
Modified function is new function. Notice how he says “loss/modification”. That said, random mutations are not Jesus, they are random while Jesus is intelligent. Random evolution is mutually exclusive with intelligent design.
Just a few years back, an article described how a lizard population was transplanted from one island in the Adriatic, to another where there were no competitors or predators, AND, no other related species of lizards. The war in Croatia intervened in any follow-up studies. After twenty or thirty years, the experimenters went back to the transplanted species of lizards and found that their behavior had changed, their jaw size had increased, and that they now had cecal valves in their stomach. These are known facts. To deny them would be to indulge in intellectual dishonesty. So, my question, dear Jerry, is this:
What caused this dramatic change in phenotype: was it duplication and divergence? Or, a SNP? Or, a recombinant event? I await your reply.
Goddidit.
I asked Jerry to answer the question. He hasn’t answered. Is this your attempt to answer the question?
Perhaps you can be a bit more specific about what lizards you were referring to. What is your understanding of the issue? Why do you expect Jerry to take the time to answer the question?
Does he owe you something?
He’s talking about the paper this article refers to:
http://scienceblogs.com/pharyngula/2008/04/still_just_a_lizard.php
money quote:
here’s the cite:
http://www.pnas.org/content/105/12/4792.short
I don’t think anyone has yet published the followup work on the specific genetics involved, but I know it’s in the works.
My understanding is not what is at issue. What is at issue is whether the commonly invoked evolutionary mechanisms can explain what we KNOW happened.
Does Jerry owe me an answer? No. He owes you and others an answer.
Here’s a question for you: is what happened on that island consistent with Darwin’s insistence on gradualism?
The above remarks were meant for Mike Haubrich.
My response can be found immediately after Ichythic’s post below.
My understanding is not what is at issue. What is at issue is whether the commonly invoked evolutionary mechanisms can explain what we KNOW happened.
Does Jerry owe me an answer? No. He owes you and others an answer.
Here’s a question for you: is what happened on that island consistent with Darwin’s insistence on gradualism?
(I’ve had to transplant this response)
Does Jerry owe me an answer? No.
since nobody else is asking inane questions about it…
How about a nice big cup of SHUT THE FUCK UP.
http://obli.net/media/1/20050818-how-about-a-nice-cup-of-shut-the-fuck-up.jpg
(I provided a picture because your reading comprehension is abysmal)
My understanding is not what is at issue.
I forgot to add:
I’m sending you a bill for my busted irony meter.
Has anyone read this paper?
http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.1
Most of it is beyond my comprehension (as I’m not a scientist), but the author appears to be arguing that protein folds are unlikely to have evolved. The paper is being touted by ID advocates as “peer-reviewed” evidence against evolution.
It’s in “Biocomplexity” FFS.
look at the “editorial team”:
http://bio-complexity.org/ojs/index.php/main/about/editorialTeam
you don’t need bother.
I’m still waiting for an answer posed in #16.
the answer is:
that’s the next part of the study – elucidating the specific genetics involved.
that it’s a novel trait in that family of lizards is unquestioned.
Ichthyic: I asked Jerry, not you.
The putative answer you provide is not an answer, but an evasion. Certainly it should be possible to apply Darwinian principles to known facts.
Your response reminds me of a question I asked a Marxist 35 years ago. When I asked him why he thought communism was superior to capitalism given that people were doing all they could to flee Russia, and all they could to sneak into the US, he responded that he would have to go back and talk to some of his fellow travelers to give me an answer. Naturally, I never heard from him again.
Certainly it should be possible to apply Darwinian principles to known facts.
it is.
they were.
it worked.
you seem to be confused as to what your question actually IS.
See, I thought your question is what you stated HERE:
“What caused this dramatic change in phenotype: was it duplication and divergence? Or, a SNP? Or, a recombinant event?”
if, OTOH, you want an analysis of the DARWINIAN mechanisms involved, which would be at the level of selection and watching traits change within populations, then that paper has already been published.
It’s the one you obliquely referred to.
didn’t you read it?
oh, wait, I’m terribly sorry; I forgot you’re a fuckwit.
my apologies.
carry on.
We don’t of course know what genetic changes caused this phenotypic change, and I THINK that we’re not even sure it’s a genetic change. It looks like one, but you’d have to rear the lizards in the lab (with the ones lacking the valve) to be sure.
At any rate, please leave off the invective (“fuckwit”). The guy is way annoying and could have found the answer himself, but surely you can counter him without the extreme name-calling.
Thx.