Behe's Test
by BilboIn his book, The Edge of Evolution; the Search for the Limits of Darwinism, Michael Behe cites work by Barry Hall in support of his view that there are limits fairly narrow limits to what Darwinian evolution can accomplish:
But antibiotics that require multiple changes are far more resistant to Darwinian processes. That's a critical fact to understand, too. Malaria requires several mutations to deal with chloroquine, so it's a far better drug than ones that are stymied by a single mutation. And chloroquine is not the only case. Recently, former University of Rochester microbiologist Barry Hall examined various antibiotics in a class called "carbapenems," which are chemically similar to penicillin.[26] With unusual clarity of thought on the topic of evolution, Hall wrote, "Instead of assuming that [the chief kind of enzyme that might destroy these antibiotics] will evolve rapidly, it would be highly desirable to accurately predict their evolution in response to carbapenem selection" (emphasis added). Using clever lab techniques he invented, he showed that, although most of the antibiotics quickly failed, one didn't. The reason is that neither single nor double point mutations to the enzyme allowed it to destroy the certain antibiotic (called "imipenem"). Wrote Hall, "The results predict, with >99.9% confidence, that even under intense selection the [enzyme] will not evolve to confer increased resistance to imipenem." In other words, more than two evolutionary steps would have to be skipped to achieve resistance, effectively ruling out Darwinian evolution.
(p.236-237).
[26] Hall, B.G. 2004. In vitro evolution predicts that the IMP-1 metallo-beta-lactamase does not have the potential to evolve increased activity against imipenem. Antimicrob. Agents Chemother. 48:1032-33.
I haven't read Hall's paper, so I'm taking Behe's word on how to interpret it. If the interpretation is correct, then it sounds like Hall is confirming where Behe thinks the edge of Darwinian evolution is. If correct, this could have profound consequences for medical research. We would only need to find drugs that require more than two evolutionary steps in order to bestow guaranteed resistance to bacteria.
Is Behe's interpretation of Hall correct? If so, is Hall right? Does that make Behe right? I'll be on vacation for a week. Please stay on topic. I'm curious what the critics have to say on this. I'll read it when I get back.
August 19th, 2008 at 3:30 pm
One thing to keep in mind is that there are higher-order forms of mutation as well. Here we are just speaking of point mutations. Hall's own research shows how insertion sequences can cause multi-base-pair sequences quickly, when a high-order mutation is being used:
Transposable elements as activators of cryptic genes in E. coli.
Comment by johnnyb — August 19, 2008 @ 3:30 pm
August 19th, 2008 at 4:25 pm
There is a huge difference between saying that:
1. one specific enzyme sequence cannot evolve increased resistance* in a lab test, and
2. saying that a whole organism's genome cannot evolve resistance in a lab test, and
3. saying that no microbes in a whole community of dozens/100s of species will not evolve resistance in a lab test (i.e. a human trial)
4. In each of the above, replace "in a lab test" with "in the wild" and then with "in the wild over tens/hundreds/millions of years"
Apart from the numerous issues with #1 (point mutations are not the only form of mutation), Behe tries to use #1 to prove #2 & #3 & #4. Which is um, well, totally bogus and frankly stupendously obviously dubious.
Plus, if you read about imipenem resistance, you soon find stuff like this:
=====
Journal of Hospital Infection (2005) 60, 19–26
Identification of an imipenem-resistant Pseudomonas aeruginosa clone among patients in a hospital in Rio de Janeiro
V.M. Kokisa, B.M. Moreiraa, F.L.P.C. Pellegrinoa, M.G. Silvaa, J.B. Longb,
C.C.R. Bastosb, K.R.N. Santosa,*
KEYWORDS
P. aeruginosa;
Imipenem resistance;
Molecular typing
Summary A total of 85 Pseudomonas aeruginosa isolates were obtained
from October 1999 to April 2000 in a tertiary care hospital in Rio de Janeiro,
Brazil. The imipenem susceptibility was evaluated by disk diffusion and agar
dilution methods, and the clonal relationship among 67 isolates was
examined by macrorestriction profile analysis following pulsed-field gel
electrophoresis. Imipenem resistance was observed in 52 (61.2%) isolates.
Imipenem-resistant P. aeruginosa isolates were separated into 10 genotypes,
73% of which belonged to genotype A. Identification of a single P.
aeruginosa clone with a high rate of imipenem resistance emphasizes the
need to control the transmission of this organism among patients.
=====
Whoops. The real question is, why do ID fans *never* check *any* of these things for themselves, and instead just lap up whatever half-baked, poorly-researched assertion an ID authority makes?
Comment by Nick Matzke — August 19, 2008 @ 4:25 pm
August 19th, 2008 at 4:37 pm
Emergence and Rapid Spread of Carbapenem Resistance during a Large and Sustained Hospital Outbreak of Multiresistant Acinetobacter baumannii
Xavier Corbella,1,* Abelardo Montero,1 Miquel Pujol,1 M. Angeles Domínguez,2 Josefina Ayats,2 M. José Argerich,1 Frederic Garrigosa,3 Javier Ariza,1 and Francesc Gudiol1
Departments of Infectious Diseases,1 Microbiology,2 and Intensive Care Medicine,3 Hospital de Bellvitge, University of Barcelona, Barcelona, Spain
link
Comment by Thought Provoker — August 19, 2008 @ 4:37 pm
August 19th, 2008 at 5:03 pm
Ah, yes, there's Nick with the tired ol' "But we've got millions of years and millions of bugs" argument.
Plus mischaracterizing Behe's point.
Plus the usual citation to some paper that supposedly has some bearing. Excuse the skepticism, Nick, but please humor us with an explanation of how, precisely, the resistent strain emerged; what mutations were involved; whether the resistance involved multiple, coordinated mutations; whether new information was achieved; and if so, whether it had anything to do with a typical Darwinian-style mechanism.
You know, surely, that Behe is not arguing against RM+NS generally, just trying to find a reasonable boundary, based on known experience and known conditions (not hypothetical "lots 'o' years, lots 'o' bugs" fantasy scenarios). If you've got good data that suggest the edge of evolution should be farther up the chain than Behe argues, then feel free to state the case in some detail. Throwing around a citation about yet another instance of some resistant bug is not particularly helpful.
Comment by Eric Anderson — August 19, 2008 @ 5:03 pm
August 19th, 2008 at 5:19 pm
Hey, don't get mad at me, Behe was the one who claimed that imipenem resistance was a case where Darwinian evolution of resistance was ruled out.
Comment by Nick Matzke — August 19, 2008 @ 5:19 pm
August 19th, 2008 at 5:53 pm
Even if we accept at face value Behe's assertion that an evolutionary step requiring two or three simultaneous mutations represents an insurmountable obstacle to Darwinian evolution, the idea was never that a species can adapt to any selective challenge. Clearly, if the selection is sufficiently strong that a population cannot adapt, it will go extinct. Take a flask with billions of bacteria and treat it with bleach, or boil it. What do you learn from the observation that none survived? Is this the edge of evolution? Is this relevant in some way to the selective pressures populations are generally faced with?
A very important question here is how well these extremely stringent selective conditions that Behe loves to throw around (e.g. chloroquine resistance in malaria, or imipenem resistance in bacteria, ect.) reflect what happens in nature. How often is a population faced with a selective pressure that will kill all but 1 in 10^20 members of the population? Not very often. Much more relevant conditions for evolution in the wild would be those that select for a variant that is 10% or 20% or even 100% better adapted to the environment than the rest of the population. It's very easy to see that modest selective pressures would be more amenable to step-wise adaptations. Why focus on such extremes?
Comment by David E Levin — August 19, 2008 @ 5:53 pm
August 19th, 2008 at 6:04 pm
Eric Anderson:
That tripped my crackpot alarm system. How does something "achieve" new information?
Comment by Raevmo — August 19, 2008 @ 6:04 pm
August 19th, 2008 at 6:16 pm
Raevmo,
It happens by random mutation coupled with natural selection. You should read about the evolution of Antarctic antifreeze proteins from a digestive enzyme called trypsin. Or try learning about the evolution of a nylon degrading enzyme from an unrelated protein. The bacterial species in this latter example "achieved" its new coding information during the last 50 years because nylon didn't exist before tlhat. There are lots of examples of the evolution of new information. You just have to be open to learning about them.
Comment by David E Levin — August 19, 2008 @ 6:16 pm
August 19th, 2008 at 6:29 pm
Nick Matzke,
Why did you leave out the part where Behe discusses the possibilities of multiple mutations? Or the fact that Behe doesn't refute the fact that resistance evolves?
Do you think misrepresenting others makes you look good? It sure doesn't make you look smart.
Good to hear from you, by the way.
Comment by chunkdz — August 19, 2008 @ 6:29 pm
August 19th, 2008 at 6:30 pm
David, thanks for opening my eyes.
You could say that selection causes a transfer of information from the environment to the populations of genomes that live in them. The presence of a new antibiotic will soon be detectable in the altered genomic content because selection favored the genomes with increased resistance. Does that sound about right?
Comment by Raevmo — August 19, 2008 @ 6:30 pm
August 19th, 2008 at 7:05 pm
Raevmo,
Sure. I don't have a problem with that characterization of how a population gains new genomic information. No evolutionist suggests intent in the process. It is, as you say, a response to the environment, which sculpts the population. What is the argument here?
Comment by David E Levin — August 19, 2008 @ 7:05 pm
August 19th, 2008 at 7:08 pm
From a CDC web site…
link (emphasis mine)
When I read Bilbo's challenge for the Behe Test, I didn't know how difficult it would be to find an example of resistance to imipenem. It wasn't difficult at all. Since that was too easy, I looked for a more specific example, imipenem resistance and metallo-beta-lactamase enzyme. I found the above.
If I am reading this correctly, this goes beyond an antibiotic resistance requiring multiple mutations to multiple antibiotic resistances requiring multiples of multiple mutations.
Time to move the goal posts?
Comment by Thought Provoker — August 19, 2008 @ 7:08 pm
August 19th, 2008 at 7:15 pm
David, we agree. I'm with the good guys here, OK? May the Force be on our side and destroy the evil worshipers of The Designer.
Comment by Raevmo — August 19, 2008 @ 7:15 pm
August 19th, 2008 at 7:24 pm
Thought Provoker,
While you have done an admirable job of showing that Behe (and Bilbo) has misplaced the goalposts, these guys have shown no reluctance in the past to simply move them. "Oh, this isn't IC because there is a simpler version? Well then, the simpler version is IC". I think it's important to acknowledge that there is a limit to what evolution can accomplish. It is limited by the genomic information available within the population and by the stringency of the selective pressure. There are undoubtedly things evolution cannot do. It has to work within certain constraints.
The real problem with Behe's construct is his assertion that most of the important evolutionary adaptations require multiple, simultaneous mutations and are, therefore, beyond the edge of evolution. This claim is completely unsupported. In fact, the very examples he uses in EoE involving the impossibility of evolving protein-protein binding sites have been shown to be bogus in the lab and in nature. This is his fatal flaw, not the claim that there are limits to what evolution can accomplish.
Comment by David E Levin — August 19, 2008 @ 7:24 pm
August 19th, 2008 at 7:29 pm
Lets see if I understand the claim: Behe argues that the X required point mutations needed to evolve imipenem resistance is impossible (or at least astronomically improbable) but the Y {Y : Y < X} point mutations needed to evolve chloroquine resistance is feasible. This assumes 1) only point mutations occur, and 2) that imipenem resistance is the only selective pressure such that evolution must happen in one step.
It was already pointed out that assumption #1 makes this conclusion not very meaningful since we know of many other evolutionary mechanisms. TP has even found evidence that this has actually evolved through some means. #2 is also not a condition that would apply to a realistic scenario. In a complex environment some of the same point mutations needed for X might be benificial against other presures. For example, consider the case where (Y ∩ X). You might first evolve all of Y due to one selective pressure and from that point evolve the remaining elements of set X (assuming X - Y <= Y) in response to another pressure.
In other words, specifying that a large number of specific point mutations cannot feasibly happen all in one step in response to a single selective presure is not a controversial statement. No one has ever claimed that happens in the first place (not that I'm aware of, at least).
Comment by Todd Berkebile — August 19, 2008 @ 7:29 pm
August 19th, 2008 at 7:33 pm
Raevmo,
Ah, sorry about the friendly fire.
Comment by David E Levin — August 19, 2008 @ 7:33 pm
August 19th, 2008 at 7:37 pm
Todd,
Exactly. The strawman argument that Behe establishes without any evidential support is that evolutionary theory predicts that multiple, simultaneous mutations are required for the evolution of even modest molecular machines even though this is too much to ask. All of the available evidence, and there is plenty, indicates that step-wise adaptation is the rule, not the exception, even when it comes to evolving things that Behe claims are beyond the limit.
Comment by David E Levin — August 19, 2008 @ 7:37 pm
August 19th, 2008 at 8:01 pm
Many who know me in real life often suggest I can be obsessive/compulsive when faced with a challenge.
Sure, I found information about imipenem and the metallo-beta-lactamase enzyme, but what about IMP-1 metallo-beta-lactamase enzyme?
It's known as "IMP-1 MBLs" by those stubborn Darwinists tracking the multiple breakouts…
link
Is this test over yet?
Comment by Thought Provoker — August 19, 2008 @ 8:01 pm
August 19th, 2008 at 8:18 pm
Let's ask the author, Barry Hall.
Many resistance genes evolve by single mutations. If it takes more than a couple of mutations (simultaneous, or each of which are not separately beneficial), then it is very unlikely nature will stumble on the solution. This isn't anything new.
Evolution is highly constrained in what it can do. If evolution wasn't constrained, Iraqi children would have Kevlar skin.
But if each mutation provides a minimal benefit, then sequential mutations can lead to ever improving fitness. By the way, Barry Hall is the author of Phylogenetic Trees Made Easy.
Comment by Zachriel — August 19, 2008 @ 8:18 pm
August 19th, 2008 at 8:20 pm
A few thoughts for those too quick to declare victory:
No-one has yet indicated how the imipenem resistance came about. Again, was it through a breaking of some pre-existing function (which Behe discusses at some length in his book and says Darwinian mechanisms can easily accomplish); was it through the triggering of a hypermutation response (which is not at all a Darwinian process)? All we have so far is a couple of citations to bugs with impipenem resistance, coupled with lazy declarations of faith in the alleged Darwinian mechanism. (I admit I remain skeptical because, in my experience, in every instance where the Darwininan mechanism is declared victorious, upon closer inspection the story inevitably breaks down to something quite unimpressive.)
I particularly like David's comment that "It's very easy to see that modest selective pressures would be more amenable to step-wise adaptations."
Right. So modest selective pressure is supposed to confer the kinds of results that significant selective pressure cannot? Sheesh, perhaps Lenski should have been subjecting all those tens of thousands of generations of fruit flies to "modest selective pressure" rather than significant selective pressure. Then perhaps it would have resulted in something of significance.
David's comments about the achievement of new information are also strained. For example, Behe discusses the antifreeze example at some length in his book. The declaration that "there are lots of examples of the evolution of new information" is nothing more than an article of faith.
Finally, as most of you know (having of course read the book you are critiquing), Behe does not ultimately claim that a couple of point mutations are beyond the edge of evolution. He uses his review of malaria et al. to establish a tentative basis for drawing the edge and is even willing to go up to the level of orders for the edge of evolution.
If this is what counts as a "refuation" of Behe's position amongst the Darwinian faithful, then we are clearly dealing with an a priori ideology, rather than a sincere attempt to understand the man's position and to honestly deal with the points he raises.
Comment by Eric Anderson — August 19, 2008 @ 8:20 pm
August 19th, 2008 at 8:34 pm
David:
Have you even read the book? I don't remember him making such a claim. Your claim that he did is itself a straw man. Unless I missed something.
Comment by fifth monarchy man — August 19, 2008 @ 8:34 pm
August 19th, 2008 at 8:47 pm
Hey,
I'm trying to stay on topic as Bilbo requested. Reread the opening post.
This is about a very specific claim, a test.
Bilbo provided a clear passage which included Hall stating…
"The results predict, with >99.9% confidence, that even under intense selection the [enzyme] will not evolve to confer increased resistance to imipenem."
And Behe summarizing…
"In other words, more than two evolutionary steps would have to be skipped to achieve resistance, effectively ruling out Darwinian evolution."
And Bilbo asking…
"Is Behe's interpretation of Hall correct? If so, is Hall right? Does that make Behe right?"
Shall we stay on topic? Do we have answers to Bilbo's questions yet?
Comment by Thought Provoker — August 19, 2008 @ 8:47 pm
August 19th, 2008 at 8:59 pm
Eric: I particularly like David's comment that "It's very easy to see that modest selective pressures would be more amenable to step-wise adaptations." So modest selective pressure is supposed to confer the kinds of results that significant selective pressure cannot?
David: Modest selection pressure will allow the selection of beneficial mutations that would otherwise be eliminated upon a more stringent selection. We see this in the lab all the time. Use a low level of selection, you get a certain constellation of mutations. Use a higher level of selection and certain of those mutations obtained in the less stringent selection fall away because the selection was too stringent. You have some conceptual problem with this fact?
Eric: David's comments about the achievement of new information are also strained. For example, Behe discusses the antifreeze example at some length in his book. The declaration that "there are lots of examples of the evolution of new information" is nothing more than an article of faith.
David: An article of faith? The fact that Behe discusses the antifreeze example does not make it less valid. You conveniently ignored the nylonase example. I have a lot more "articles of faith". Would you care to discuss them?
Eric: Behe does not ultimately claim that a couple of point mutations are beyond the edge of evolution. He uses his review of malaria et al. to establish a tentative basis for drawing the edge and is even willing to go up to the level of orders for the edge of evolution.
David: Sure. But he uses the same flawed logic that the most important adaptive changes require multiple simultaneous mutations, a clain for which there is zero evidential support.
Comment by David E Levin — August 19, 2008 @ 8:59 pm
August 19th, 2008 at 9:07 pm
Thanks, TP, for keeping us on topic.
I don't think we have the answer to Bilbo's second question yet, as it isn't clear whether the cited papers are relevant to the question.
Specifically, Behe is citing an evolutionary proponent (Hall) to support the idea that when more than two evolutionary steps have to be skipped, even under intense selection there is a >99.9% certainty that resistance will not evolve. Behe is *not* saying that imipenem resistance cannot evolve. He is simply pointing out that others in the field recognize the need for a slight, successive, beneficial pathway. Let me say that again: Behe is not saying that imipenem resistance cannot evolve. Thus, Nick's quick citation of a paper referring to imipenem resistance as a victory dance is both off topic and off base. As is his statement that "Behe was the one who claimed that imipenem resistance was a case where Darwinian evolution of resistance was ruled out." No Behe didn't. Again, another example of failure to refute, because Behe's original point was not even engaged.
It seems that Behe is interpreting Hall correctly, for the specific point he is trying to make. Thus, the answer to Q1 is yes. Q2: Is hall right? I don't know, but the cited papers give me no confidence that Hall is wrong. We haven't even identified yet in this thread how the resistance came about, much less whether it involves a Darwinian mechanism and whether it involves skipping "more than two evolutionary steps".
Q3 is more of a logical follow-on: If Hall is right, it will certainly be an example in support of Behe's efforts to locate the edge of evolution. If Hall is wrong, then Behe will have to look elsewhere for examples, and it may even be a case against Behe's point.
Comment by Eric Anderson — August 19, 2008 @ 9:07 pm
August 19th, 2008 at 9:18 pm
FMM,
His basic premise is that the evolution of certain very fundamental things in the cell, such as new protein-protein binding sites, requires multiple, simultaneous mutations, which are extemely unlikely to happen by natural means.
From EoE, page 135: "Generating a single new cellular protein-protein binding site is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite".
This bogus assertion is based on his completely unjustified claim that a new binding site would require 5 or 6 simultaneous mutations before any selective advantage arises. This is a strawman argument, because the evolution of new protein-protein binding sites does not require any such thing. His assertion ignores the role of step-wise mutation in this process.
Oh, and yes. I read the book. There are lots of other examples that support my claim of his strawman argument. Would you like some more?
Comment by David E Levin — August 19, 2008 @ 9:18 pm
August 19th, 2008 at 9:21 pm
David wrote:
"Sure. But he uses the same flawed logic that the most important adaptive changes require multiple simultaneous mutations, a clain for which there is zero evidential support."
That is not an accurate statement. It is you who have "zero evidential support" for the idea that "the most important adaptive changes" do not require multiple simultaneous changes. The slow, adaptive chain of events leading inexorably to any of the "most important adaptive changes" (new cell types, organs, body plans, etc.) has never been demonstrated in any lab or in the wild and exists only in the minds of certain individuals.
If we take the question as an empirical one, based on current knowledge, it is clear that the key characteristics (cells, organs, body plans) require a multitude of coordinated and simultaneously existing systems. That is an empirical fact, based on the current structure of the systems, that can be evaluated today by looking at the system in question.
If we look instead at the historical question of how the system came about, that is a more tenuous question, as no-one was there at the time and we have no direct observation. The best anyone (Behe, you, me, or anyone else) can do is draw an inference as to what is likely to have occurred. Behe argues, given the current examples we have, that it is exceedingly unlikely that these systems could arise without a multitude of coordinated changes. One can dispute Behe, but it will need to be on the basis of actual evidence, not statements of faith in an alleged historical mechanism that somehow doesn't seem to be currently operative.
Comment by Eric Anderson — August 19, 2008 @ 9:21 pm
August 19th, 2008 at 9:24 pm
David, I'm just trying to understand: what is this "step-wise" mutation idea you keep referring to?
If it is just the idea that several mutations can build upon each other with successive increases in fitness, then it seems you are really talking about Darwin's "slight, successive" modifications idea. Behe is not building a straw man around this. He is questioning it head on with the idea that some systems require multiple coordinated changes.
If you are referring to co-option or some other idea, it is not clear how that helps the picture at all.
Comment by Eric Anderson — August 19, 2008 @ 9:24 pm
August 19th, 2008 at 9:32 pm
Eric,
In fact, using Behe's own example of the impossibility of evolving new protein-protein binding sites, we can demonstrate the fallacious nature of his argument. There are very good examples of the evolution of protein-protein interactions in the lab. A single mutation allows for a weak interaction, a second mutation strengthens the interaction, etc. Iterative rounds of selection can yield a very strong interaction relatively quickly. This is not a problem, but Behe ignores it completely. Something else he ignores is in his careful description of the evolution of the antifreeze protein. This is the fact that the new protein is enzymatically modified with sugar residues. How does this happen? Through a new protein-protein interaction. Oooops! It's interesting that he leaves out that particular detail, but otherwise gets the story pretty much correct. Intellectual dishonesty.
Comment by David E Levin — August 19, 2008 @ 9:32 pm
August 19th, 2008 at 9:38 pm
Eric,
Indeed, he is asserting that it is not possible to build protein complexes because even a single new protein-protein interaction is extremely unlikely to arise. This is based on a presumed requirement for multiple simultaneous mutations. He makes a very broad assertion as an extension of the extreme example of chloroquine resistance, as though this is somehow representative of the way selective pressures drive evolution in the wild. This is his strawman. We know that protein-protein interactions evolve in the lab and in nature and that it happens one mutation at a time.
Comment by David E Levin — August 19, 2008 @ 9:38 pm
August 19th, 2008 at 9:45 pm
Hi Eric,
Thank you for your on topic response.
However, I suggest that you have misplaced which parts of the opening post go to which questions. The quote…
"In other words, more than two evolutionary steps would have to be skipped to achieve resistance, effectively ruling out Darwinian evolution."
…were Behe's words, not Hall's. They are applicable to either Q1 or Q3. It has nothing to do with Q2.
I would argue that Behe presented this as a truism. The concept is certainly consistent with the theme of his book, The Edge of Evolution. It is almost certainly what Bilbo intended when he asked his third questions, otherwise there is nothing for Behe to be "right" about.
However, in light of the available evidence that resistance was achieved, I can understand why a firm statement about what "….would HAVE TO BE skipped to achieve resistance' might be a little embarrising. (my bold)
Something has to give. Either Behe was wrong and/or Hall was wrong and/or Behe's interpretation of Hall was wrong.
Either that, or the resistance to imipenem is proof multiple evolutionary steps can be skipped in nature.
I will be curious to see if your next move ends up implying the multiple steps needed to make the bacteria more deadly were, in fact, skipped as the designer intended.
Comment by Thought Provoker — August 19, 2008 @ 9:45 pm
August 19th, 2008 at 10:25 pm
Well heck if you/he admit that resistance in question (to imipenem) evolves, then the origin of imipenem resistance is not a failed "test" of standard evolutionary theory and the whole example is pointless except as an observation that strengthens standard evolutionary theory.
PS: Behe's whole discussion, and this thread, are I think based on another misunderstanding. Hall's paper is about the evolution of *increased* resistance. IIRC IMP-1 already confers a significant amount of resistance, as do various related enzymes (but I haven't read this stuff since 2005 when Behe started this line of argument so it's all IIRC). So Hall never claimed that imipenem resistance couldn't evolve, he just claimed that this particular-already-optimized-enzyme couldn't get even better in this specific way (point mutations).
Behe & fans, however, appear to have misread Hall to say that imipenem resistance couldn't evolve at all, or at least is wildly improbable.
Comment by Nick Matzke — August 19, 2008 @ 10:25 pm
August 19th, 2008 at 10:40 pm
Eric Anderson:
If Behe is looking for an edge he might stick close to models that link changes in amino acid sequence to protein folding and consequent changes in protein structure. Unstructured intermediates are not at all uncommon and accurate predictions correlating sequence changes, structural changes and effects on function show where the edge lies. Functional transition possibilities can depend on the nature of folds which in turn is affected by encoded sequences.
Comment by Bradford — August 19, 2008 @ 10:40 pm
August 19th, 2008 at 10:41 pm
Focusing on the questions Bilbo asked. (Did I mention that I can be obsessive/compulsive)…
Here is Hall's paper mentioned in the opening post. It ends with the following summary…
link
While Hall provided a lot of qualifiers, we can see with 20/20 hindsight that it was still rather bold. While other MBL subfamilies did evolve too, IMP-1 was specifically fingered in a blast (see previous comment with IMP-1 example).
The Status Quo consensus would probably agree with Hall's suggestion that a lack of instrument sensitivity could cause incorrect results. Either, that, or an incorrect analysis of probabilities.
The challenging (ID) consensus would probably be that processes, unrecognized by mainstream scientists, came into play.
Either way, it seems that Hall specifically was rejecting the idea that this study should cause a challenge to current thinking or that if resistance appeared it would "HAVE TO" mean anything significant.
My suggested answer to Bilbo's second question is a qualified "Hall was not wrong but his study's results suggested an incorrect conclusion".
Behe was clearly NOT correctly summarizing Hall's conclusion with "In other words, more than two evolutionary steps would have to be skipped to achieve resistance, effectively ruling out Darwinian evolution."
Either the answer to the first question is "Behe's interpretation of Hall was incorrect" or Behe has made his own specific claim as to what the appearence of imipenem resistance means.
Comment by Thought Provoker — August 19, 2008 @ 10:41 pm
August 19th, 2008 at 10:57 pm
More on topic discussions concerning Bilbo's questions. Here is something to note when considering whether or not Behe correctly represented Hall's paper…
From Hall's paper Behe referenced.
Comment by Thought Provoker — August 19, 2008 @ 10:57 pm
August 19th, 2008 at 11:56 pm
Nick Matzke:
So there is an edge Behe is seeking.
Comment by Bradford — August 19, 2008 @ 11:56 pm
August 20th, 2008 at 12:00 am
TP:
Not so. "The possibility that increased resistance, below the level of laboratory detection, could be selected in nature," does not indicate an incorrect conclusion, only a possibility within a specified detection level.
Comment by Bradford — August 20, 2008 @ 12:00 am
August 20th, 2008 at 12:10 am
Nick Matzke:
So… Hall didn't really mean it when he said…
…even with the caveats and back wall cracks? 99.9% looks fairly confident to me. But regardless, Behe didn't say it couldn't evolve "at all," he said it was 99.9% unlikely to evolve by mechanisms known for "Darwinian evolution."
It's actually okay to say that in public these days. 'Everybody knows' evolution isn't looking very Darwinian of late. You don't have to rely on straw men and misrepresentations anymore.
Comment by Joy — August 20, 2008 @ 12:10 am
August 20th, 2008 at 7:28 am
Bradford,
So what? Nobody argues that there is not a limit to what evolution can do. It will never create fire-breathing dragons either, but this is no argument against the evolution of one form of life into another one mutational step at a time. Certainly any adaptation that can only arise through several simulataneous mutations (without individual benefit from any) will be a challenge to evolution. However, there is no evidence that such extreme adaptations are of any significance in nature. Behe's "edge" is no edge at all; it's an artificial construct with no relevance to evolution in the wild.
Comment by David E Levin — August 20, 2008 @ 7:28 am
August 20th, 2008 at 8:44 am
Hi Bradford,
The incorrect conclusion was "…the risks associated with the presence of blaIMP-1 do not include the risk of evolving increased activity against imipenem."
The reason Hall was not wrong, is because the study's result clearly indicated that incorrect conclusion but, on the other hand, Hall clearly allowed for "…the possibility that increased resistance, below the level of laboratory detection, could be selected in nature."
Behe didn't communicate that as clearly as Hall did.
Comment by Thought Provoker — August 20, 2008 @ 8:44 am
August 20th, 2008 at 9:27 am
Keeping the focus on Bilbo's three questions.
Q1 is still being discussed.
The facts for Q2 ("is Hall right?") are becoming clearer. I still stand by my qualified answer of "Hall was not wrong but his study's results suggested an incorrect conclusion".
Upon reflection I suggest the answer to Q3 ("Does that make Behe right?") is a clear negative.
The answer to Bilbo's third question involves two parts. The first being the presumption Behe is right, the second being does Hall's study's result show that Behe is right.
The answer to the question "My pregnent wife is eating sugar cookies, does that mean she will have a girl?" is an unqualified negative regardless of whether she will have a girl or not.
Neither Hall's presumption that "…the possibility that increased resistance, below the level of laboratory detection, could be selected in nature" nor the incorrect conclusion coming from the study's results support's Behe's presumption concernting an "edge" to evolution.
It may be supportive of Behe's caveats, but that is a reverse ad homenem. It is like saying "Behe is right about the truth of common descent, therefore Irreducable Complexity is a fact".
Ergo, my proposed answers to Bilbo's questions…
A2. "Hall was not wrong but his study's results suggested an incorrect conclusion".
A3. Behe may or may not be right, but Hall's paper does not “make Behe right”.
Still working on the first question. I think that will boil down to whether Behe was trying to interpret Hall’s position or coming to his own conclusion when he said…
“In other words, more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution.”
…because it is difficult to see how that is a correct interpretation of what Hall was saying.
Comment by Thought Provoker — August 20, 2008 @ 9:27 am
August 20th, 2008 at 11:01 am
It is a matter of frustration that rather than engaging in serious discussion about the claims of the book (i.e. that there is an edge to what evolution can achieve), opponents of ID concentrate on quibbling with details. Rather than saying, "Ah, well Behe's edge doesn't work in this case" (as often as not by case-mining), why not say, "The concept of an edge of evolution" (which is what the real problem is in darwinian terms, after all) "is irrelevant, because …. neutral mutations are a lot more widespread than we thought." Or whatever. It is the concept itself which needs to be invalidated, not specific cases.
The darwinist approach isn't substantially removed from saying "The fact that he spelt that word wrong invalidates his whole argument."
Comment by Exile From Groggs — August 20, 2008 @ 11:01 am
August 20th, 2008 at 12:01 pm
The thread topic concerns the particular case.
The fact that not every conceivable option is available to evolutionary processes is irrelevant, as the Theory of Evolution doesn't make that claim. Rather, the progress of evolutionary adaptation is highly constrained by its history. However, when we look at the overall historical pattern, we see Common Descent and a variety of transitional and intermediate organisms and structures. Fins to legs to arms to wings to fins.
Comment by Zachriel — August 20, 2008 @ 12:01 pm
August 20th, 2008 at 12:06 pm
Exile from Groggs commented…
If this was directed to me and my comments, pleased reread Bilbo's opening post. Bilbo asked three specific questions about a specific excerpt of Behe's book.
Q1. "Is Behe's interpretation of Hall correct?"
A1. It depends on whether or not the declaration that "…more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution” was Behe's own claim or Behe's interpretation of what Hall was claiming.
Q2. "If so, is Hall right?"
A2. Hall was not wrong but his study's results suggested an incorrect conclusion.
Q3. "Does that make Behe right?"
A3. Behe may or may not be right, but Hall's paper does not “make Behe right”.
One Bilbo make the specific request to "Please stay on topic."
I am staying on topic. I suggest arguing about the pros and cons of Behe's view in general isn't staying on topic.
Comment by Thought Provoker — August 20, 2008 @ 12:06 pm
August 20th, 2008 at 1:07 pm
The arguments here all seem to be at the level of how many angels can dance on the head of a pin. What Behe did was look at a well studied fast reproducer under various selection pressures to see what positive results were produced by trial and error. What he found was entirely within the bounds of what statistical mechanics predicted given a base mutation rate and number of opportunities for heritable change to occur. In a real life study physics and population genetics came through with flying colors.
The problem comes about when we apply the same principles to indirectly observed populations evolving over time where we don't have the benefit of sequence analysis. One case in point is the evolutinary change from reptiles to mammals. In this case there are far more novel adaptations in evidence where said adaptations require far more in the way of novelty than a few or even a few score of serendipitous stepping stone modifications discovered by trial and error. To add insult to injury these modifications happened with far fewer opportunities for heritable change.
The predicted and now confirmed capacity of mutation & selection is simply inadequate to explain the fossil record. The only reasonable explanation copacetic with common descent is that creative evolution proceeded along a more or less predetermined trajectory where the rudiments of complex biological structures were already built into the genome and/or epigenome of the evolving cell lines and where they were easily accessable to a brute force trial & error discovery mechanism. In essence this explanation is what Mike Gene describes and supports in far greater detail in "The Design Matrix" which is a book that should be required reading for anyone taking a contrary position with regard to intelligent design. I'd also put on that required reading list Behe's "Edge of Evolution" and Sanford's "Genetic Entropy". The numbers and principles put forward in those tomes all hold true in real life observation of evolution by chance & necessity. Where they don't work out is explaining the evolutionary sequence observed in the indisputable testimony of the fossil record. Evolution by chance & necessity only works when no one is observing it. When not being closely scrutinized it takes on what can only be described as miraculous powers to overcome statistical constraints. There are fewer than two degress of difference between God of the Gaps and Chance of the Gaps. The gaps are real and chance can't fill them except in the imagination.
Comment by DaveScot — August 20, 2008 @ 1:07 pm
August 20th, 2008 at 1:31 pm
Is there a specific trait you think could not evolve?
Comment by Zachriel — August 20, 2008 @ 1:31 pm
August 20th, 2008 at 1:33 pm
TP wrote:
You have left out a possibility, and frankly, perhaps the most likely possibility. You are wrong to state that "resistance to imipenem is proof that multiple evolutionary steps can be skipped in nature." We still have not determined how the imipenem resistance came about in the cited cases. I am getting blue in the face, but again I ask: was it the result of multiple, simultaneous, coordinated mutations? If so, Hall is wrong and Behe's case is weakened. In contrast, if it was the result of a breaking of a pre-existing system, or if it was the result of slight, successive, incrementally-beneficial changes, then it is completely and totally irrelevant to the point Behe raises.
Why is this difficult to understand? Behe doesn't care a fig about imipenem resistance, and the existence or lack of imipenem resistance in nature is itself irrelevant to Behe's argument (unless it is demonsrated that it came about as discussed above). Behe's only point in bringing up imipenem in the first place is to point to another researcher who acknowledges that multiple, coordinated mutations are likely beyond what evolution can reasonably achieve. That is it.
I don't know if Bilbo's post poses a false-dichotomy-type set of questions that is causing a misreading of what Behe said. If so, be that as it may. In either case, let's try to understand what Behe actually said and what his point was.
Comment by Eric Anderson — August 20, 2008 @ 1:33 pm
August 20th, 2008 at 1:34 pm
DaveScot,
This is an unsupported assertion. We now know that wide-ranging developmental alterations that lead to striking morphological changes can arise as a consequence of a very small number of mutations in developmental regulatory genes.
Another completely unsupported assertion.
Comment by David E Levin — August 20, 2008 @ 1:34 pm
August 20th, 2008 at 1:41 pm
Zachriel wrote to DaveScot:
"Is there a specific trait you think could not evolve?"
This gets tiresome, but is there a specific trait you think could evolve and can you demonstrate that it did? On the second part, no, of course not. The grand claim — the claim that requires grand evidence — is that all these traits came about through some unguided, unplanned, naturalistic and materialistic process. The burden of proof is clearly on the folks who propound this kind of hypothesis. Youc comment underscores that this entire debate is diffused with an unholy aura which is absent in every field of real science. In real science the scientist is required to demonstrate the validity of his proposition. In evolutionary biology, the scientist is permitted to waive the magic wand and then the burden is somehow supposedly on the skeptic to demonstrate the universal negative — that it couldn't possibly have evolved.
T'ain't the way real science operates.
Comment by Eric Anderson — August 20, 2008 @ 1:41 pm
August 20th, 2008 at 1:43 pm
Eric,
I think you are correct in this. Where Behe make his fatal error in logic though is in the assertion that such multiple, coordinated mutations are necessary for evolutionary paths in the wild. There is no evidence to support such a requirement. In fact, selection of antibiotic resistance imposes such a stringent selection that it hardly represents the sort of selective pressures that a population would ever see in the wild (except when humans are trying to extinguish them).
Comment by David E Levin — August 20, 2008 @ 1:43 pm
August 20th, 2008 at 1:44 pm
It looks like Bilbo's thread has generated enough visibility to motivate DaveScot to attempt a rescue with distractions.
Unfortunately, it looks like others are taking DaveScot's bait.
Comment by Thought Provoker — August 20, 2008 @ 1:44 pm
August 20th, 2008 at 1:48 pm
My last post for a while today (gotta get back to work sometime) (:
David wrote:
David, you play in the currency of generalities and vagaries. "Step-wise mutations." "Striking morphological changes."
Let's acknowledge the facts: no significant biological systems have ever been demonstrated to have arisen through a mutational process operating in the Darwinian fashion. In my experience, the expressions of awe at the power of evolution evaporate every single time the details are pressed. If you have any specific examples of the kinds of things Behe says are beyond the edge of evolution (cell types, integrated protein networks, genetic programs, genetic code, cells, etc.), please cite them. Otherwise, your vague references to all the wonderful "striking changes" resulting from mutations are just declarations of faith.
Comment by Eric Anderson — August 20, 2008 @ 1:48 pm
August 20th, 2008 at 1:51 pm
Hi Eric,
It was neither Hall nor I who stated…
"…more than two evolutionary steps would have to be skipped to achieve [imipenem] resistance, effectively ruling out Darwinian evolution."
It was Behe.
Either it was Behe's incorrect interpretation of what Hall wrote (answering Bilbo's first question) or it was Behe's own declaration of a truism which would go to Bilbo's third question.
Shall we stay on topic as Bilbo requested?
Comment by Thought Provoker — August 20, 2008 @ 1:51 pm
August 20th, 2008 at 1:57 pm
Eric,
Indeed. A great many things have been demonstrated that support evolutionary theory. Many other things remain unknown for now, but are consistent with evolutionary theory. However, nothing is known that would refute evolutionary theory. On the other side, what sort of evidence has been provided to support ID? None. Zero. So, as you wrote, in real science the scientist is required to demonstrate the validity of his proposition. ID is nowhere to be found on the playing field of science.
Comment by David E Levin — August 20, 2008 @ 1:57 pm
August 20th, 2008 at 2:30 pm
ID proponents/Behe supporters, et al, please reread Zachariel's comment from Aug. 19th.
http://telicthoughts.com/behes...
Behe argues this in EoE and in his theoretical paper with Snoke.
http://www.proteinscience.org/...
There is an edge.
Behe's point yet again.
Zachriel seems to be reading Hall as Behe did and concludes that a feature which requires three or more, simultaneous or sequential, single-point mutations will likely not evolve. Unless each step is beneficial then natural selection cannot work to preserve it.
This is the essence both of EoE and IC.
And DaveScot was not changing the subject, he was clarifying it. Behe is presenting challenges to Darwinian evolution and demonstrating its boundaries - he is not disproving it. When he suggests that X number of organisms in Y generations will not evolve a complex feature (as defined by Behe - please, no strawmen) it is silly to say in rebuttal that there were more than X and the generations were greater than Y.
So be it.
But in an population where there are less than X and Y then we can not expect a feature of similar complexity to arise by Darwinian means.
Behe is feeding us bites, not the whole elephant. As with "evolution", the case is cumulative with many lines of evidence. We don't have one proof of MET and we won't have one refutation of it.
Comment by Pez — August 20, 2008 @ 2:30 pm
August 20th, 2008 at 2:41 pm
TP, you've done an admirable job of trying to police the thread in Bilbo's absence. But now that it's got more than 60 comments, I think there's plenty of material addressing the actual questions from you and others for him to work with when he gets back two weeks from yesterday or so.
At this point it can go another 300 comments past pertinence. It doesn't really matter - his library had excellent fast-access broadband.
Comment by Joy — August 20, 2008 @ 2:41 pm
August 20th, 2008 at 2:44 pm
Eric,
The evolution of the blood clotting cascade is a very good example. This is a pathway that Behe specifically insists is IC and therefore, could not have evolved. When we look at the blood clotting cascade in the vertebrate lineage, a very interesting progression emerges. In going from amphioxus to jawless fish to jawed fish to land vertebrates we see an increase in complexity of the clotting cascade:
http://www.pandasthumb.org/arc...
While it is not possible at this time to reconstruct a step-by-step evolutionary pathway for this cascade, the outline for its increased complexity as we go from primative chordates to land vertebrates (in order of evolutionary emergence) is clear.
Comment by David E Levin — August 20, 2008 @ 2:44 pm
August 20th, 2008 at 3:05 pm
Zach
A plethora of traits which must have all evolved is the question. We'd need someone expert in comparative anatomy to list them all. Some of them that come to mind are (mammal vs. reptile):
warm-blooded vs. cold blooded metabolism
urea vs. uric acid as end product of protein metabolism
separate bowel/urinary openings vs. cloaca
4-chambered vs. 3-chambered heart
mammary glands vs. yolk sack
neo-cortex vs. nothing
hair vs. scales
umbilical cord vs. nothing
Comment by DaveScot — August 20, 2008 @ 3:05 pm
August 20th, 2008 at 3:20 pm
Hi Bilbo,
Relying on my memory, Behe in Edge of Evolution considers the likelihood of mutations other than single-nucleotide substitutions producing the equivalent of more than two point mutations simultaneously. Though such mutations occur much rarely. I remember Behe suggesting that these mutations can't be the typical ones for darwinian evolution. Point mutations on the other hand occur much more frequently relative to other mutations. So point mutations are the best means of variation that darwinian evolution could depend on. Thus Behe focuses mainly on it.
Behe is not ruling out the possibility of mutations other than point mutations helping bacterial resistance- but since they occur rarely and are more likely to be deleterious it is not the best place to look for evidence of a typical evolutionary step. But it should be acknowledged that in Nature it is not like that. All kinds of mutations should be taken in to account before pronouncing something significant. Given this, I cannot imagine why one would argue that bacterial resistance cannot evolve when two or more evolutionary steps is needed. I don't remember whether Behe qualified his assertion preceding your quote(unfortunately, I don't have the book with me at the moment):
Here it seems Behe is assuming that the only mutations allowed for "Darwinian" evolution to occur is the more frequent point mutation. However, Modern Evolutionary Theory would include all the other kinds of mutations as its means of variation, presumably.
As others have found papers reporting the development of resistance, this seems to be not the case. However, it all depends on the how this resistance came about.
Regarding Thought Provoker's cite, do we know what type of mutations produced this resistance? Are these the type of point mutations Behe is asserting cannot develop resistance? If they are, then I think Behe's assertion is falsified. If they are not simple point mutations then Behe is not to be called on it. For he had (I think) granted the possibility that other mutations could do the job.
I'm going to read the Pseudomonas aeruginosa resistance more carefully to try to find anything significant relating to this. That cite was interesting 'cause I had to culture those suckers as part of my lab techniques practical class! Thanks TP.
Comment by samsen — August 20, 2008 @ 3:20 pm
August 20th, 2008 at 3:21 pm
David,
You do know that Behe never claimed Christmas Factor (Factor IX) to be part of the blood clotting cascade that he claimed to be IC.
So, showing that the jawless fish doesn't have Christmas Factor doesn't really do much to his claim.
From DBB:
and….
Look at the chart on the link, David.
Factor V (proaccelerin) is a co-factor. All the chart shows is the replacement of Factor V, with something like Factor V.
Sure, the jawless fish is doing quite well with out Factor V…. but look what it does have.
Again, Christmas Factor wasn't even included in the IC portion of the clotting cascade as stated by Behe…. who you are criticizing.
Comment by Doug — August 20, 2008 @ 3:21 pm
August 20th, 2008 at 3:33 pm
Nick Matzke,
I believe Behe is merely trying to see what the limits of a purely Darwinian approach are, just as many other scientists are attempting to do so that they can make better drugs faster and cheaper and so on.
Establishing the limit for what Darwinian evolution can do does not mean evolution doesn't happen, it means there might be a more focused, intelligent, or directed mechanism for evolution at work. This could be purely endogenous, front loaded, or external - nobody knows.
Now if you want to claim that Darwinian evolution includes the current synthesis AND ALSO any other mechanisms found in the future, then go for it. You'll have the dubious and hollow honor of being right no matter what should happen to be discovered in the future. However, I believe Popper would not classify that as science, but something else entirely.
Comment by chunkdz — August 20, 2008 @ 3:33 pm
August 20th, 2008 at 3:34 pm
David Levin
Are you channeling Haekel? Ontogeny does not recapitulate phylogeny. Even you should know that. You must be unconsciously channeling the notorious saltationist Richard Goldschmidt. Good. I consider it progress when a gradualist acknowledges the so-called trade secret of paleontology. The existence of switches that steer ontogenesis between disparate but functional developmental pathways raises the question of which came first - the switches or the pathways? This is evidence in favor of design not against. For the switch to be of any use there must be working pathways to switch between.
Comment by DaveScot — August 20, 2008 @ 3:34 pm
August 20th, 2008 at 3:48 pm
Helpful reading re my previous comment:
Return of the Hopeful Monster
by Stephen Jay Gould
Universal genome in the origin of metazoa: thoughts about evolution. by Michael Shermer
I'm amazed Shermer made it through peer review as I can't find the obligatory denunciation of intelligent design in his paper.
Comment by DaveScot — August 20, 2008 @ 3:48 pm
August 20th, 2008 at 4:14 pm
TP:
It looks to me like others are proving Dave Scot's original claims correct. TP, you correctly tried to keep the blog entry topical. But look at this. Quoting Dave:
He is right on target with that last sentence. We generally don't have the benefit that a specific experiment is able to highlight- reference to specific sequential changes. We must speculate instead based on our best analysis. Dave's first sentence looks to me like a charge of excessive vagueness and evidence not dependent on specific data. Yet the responses to Dave have been challenges to cite something that cannot evolve. That reduces critiques of Behe to: Don't bother with specific studies because we know that x evolves anyway to become whatever. If MET explains everything then you can fold up your tent and go home.
Comment by Bradford — August 20, 2008 @ 4:14 pm
August 20th, 2008 at 4:19 pm
There is strong evidence of the evolution of many traits. Nylonase. Hominid bipedalism. Mammalian ossicles. Cetacean skeletal adaptations. Finch diversification on the Galápagos.
To understand the evidence, you have to start with Common Descent, of course. From this we can note the basic pattern of change, and how those changes relate to the environment. And it's because the overall pattern is so strong, that we can claim with reasonable certainty that the pattern applies generally, leading to testable predictions.
DaveScot made a negative claim, hence my question.
That is roughly correct for the evolution of bacterial resistance. Of course, there are other types of genetic changes, such as frame-shifts, inversions, horizontal transfer, or recombination. It gets a bit more complicated when we consider drift.
The equivocation on "edge" is highly misleading. You can't walk through a tree in the woods, but you can walk through the woods. Behe is erecting a strawman, which you encapsulate here.
Just because one particular trait may not evolve, doesn't mean other complex traits can't evolve. No one is suggesting that cosmically rare mutations are the source of evolutionary variation. Rather, there are a series of selectable variations. For many organisms, we have good records of these selectable pathways, especially bony structures. The evidence for molecular evolution is less direct, but still convincing.
Comment by Zachriel — August 20, 2008 @ 4:19 pm
August 20th, 2008 at 4:25 pm
David E Levin:
There's an edge to evolution? Where? If it's just random variation sifted by happenstance (selection), I see no reason why it couldn't have produced fire breathing dragons. Or unicorns. Or hobbits, cave trolls, gremlins, gnomes, leprechauns and/or Sasquatch. Now, dragons probably couldn't fly if they were heavier than pterodactyls, and aren't likely to have had wings and forelimbs at the same time anyway, but dragons are walking the earth today. They don't mix volatile chemicals in order to spit fire, but they're plenty deadly anyway. An interior volatile chemical factory isn't beyond conceivability.
And this gradualism you espouse… how does it account for the evidence in the rocks of long periods of clade stability punctuated by short bursts of rapid evolution of new forms?
It wouldn't challenge evolution, it would just challenge the Darwinian/Neo-Darwinian version that insists on "one mutational step at a time," each of which must contribute to selectable fitness. I seem to recall that 'Selection Neutral' variation is common enough to be accepted these days by the rank and file. Of course, later mutations that suddenly turn neutral pieces-parts into fine-tuned IC machines does tend to suggest foresight more than opportunism, but an individual could choose to ignore such indicators of teleology and still do good science.
Is anyone looking for "such extreme adaptations," or are they all assuming as you do that these things can't happen? You tell us your theoretic can't tolerate extreme adaptations, coordinated mutational events and expression suiting, or the possibility of any organism that hasn't already existed at some point (and been duly deconstructed) ever existing at all.
I mean, wouldn't it be dumb for a researcher to spend valuable time and funding seeking phlogiston when his governing theoretic needs no such 'stuff' to explain combustion and he doesn't believe it exists? Thus your assertion that there is no evidence that extreme adaptations are significant in nature is a complete Duh.
You don't like where Behe's looking for this 'edge', but you have admitted that there is a limit to what evolution can do - an 'edge' of evolution. The construct is as artificial as all hypotheses in science are (just mind-games, though it's arguable that those are actually "artificial"), precisely as artificial as any hypothesis you could offer as to where the edge of evolution resides.
So… are you telling us that hypotheses and theories about life and evolution have no relevance to life and evolution in vivo? If so, have you considered what that means for your precious RM-NS?
Comment by Joy — August 20, 2008 @ 4:25 pm
August 20th, 2008 at 4:27 pm
Perhaps you could take one of your examples, such as the multi-chambered heart, and explain why you think there is no plausible evolutionary pathway.
Comment by Zachriel — August 20, 2008 @ 4:27 pm
August 20th, 2008 at 4:32 pm
Developmental genes has nothing to do with "recapitulation". For instance, Homeotic genes control segmentation in metazoa.
Comment by Zachriel — August 20, 2008 @ 4:32 pm
August 20th, 2008 at 4:51 pm
David E Levin,
Why?
Comment by chunkdz — August 20, 2008 @ 4:51 pm
August 20th, 2008 at 4:55 pm
Zach,
Behe would agree. What's your point?
Comment by chunkdz — August 20, 2008 @ 4:55 pm
August 20th, 2008 at 5:03 pm
Because I was responding to Eric Anderson, who apparently does not agree.
Because evolution is limited by its history and by the variation in a population.
Comment by Zachriel — August 20, 2008 @ 5:03 pm
August 20th, 2008 at 5:11 pm
So, this explains why there will never be fire-breathing dragons?
Comment by Doug — August 20, 2008 @ 5:11 pm
August 20th, 2008 at 5:53 pm
Joy,
Well, for one thing, asbestos lungs would have to evolve as well….
Punctuated equilibrium is just another description of gradualism. When you say "short bursts of rapid evolution", this is still happening in geologic time. Not, for example, thousands or tens of thousands of years; within the resolution of geologic layers.
It is Behe who is trying to find some evolutionary limit in these extreme selections that kill all but the rarest of mutants. The problem is not the assumption that they can't happen, its that there is no need to postulate that multiple, simultaneous mutations are required for the typical evolutionary adaptation. What is the rationale for this claim? Where is the evidence to support it? If the ID proponents think this is how it happens, let them generate some evidential support. Evolutionists have a well-worked out mechanism for how this happens. It is the job of the ID proponents to bring their ideas into the realm of science.
No. I don't like his inappropriate extension of this "edge" to evolution in the wild. As I wrote before, of what significance is a selective pressure that is so stringent as to kill off all but 1 in 10^20 members of a population? No evolutionist argues that this is a good proxy for selective pressures in the wild.
Comment by David E Levin — August 20, 2008 @ 5:53 pm
August 20th, 2008 at 6:21 pm
Joy:
Do you have any evidence for mutations that "turn neutral pieces-parts into fine-tuned IC machines"?
Comment by Raevmo — August 20, 2008 @ 6:21 pm
August 20th, 2008 at 6:22 pm
David E Levin:
Oh, don't tell me you don't keep up with dragon movies! They figured it out years ago. Glands on either side of the throat storing chemicals synthesized in the usual biological way, that are secreted on demand like venom - in a particular attack response. Think bombardier beetles, combined with chemical weaponry in spitting dinosaurs and some reptiles today. They never need inhale the chemicals into their own lungs. Evolution has created such oddities. There's no reason to think it couldn't happen, even if it never did. Evolution explains all!
Yeah. We have nearly 600 million years to work with, during which time every visible creature to have walked the earth lived and died and contributed (or didn't) to the gene pool and the fossil record. A few million here, a few million there, pretty soon you're talking real Deep Time. "Rapid" is a relative term, based on the regular appearance of new forms that we see all around us today as life pops into existence in mudholes everywhere every time it rains… [/snark]
You know, it wouldn't hurt you to check some of your stereotypes at the door, since this is TT and not AIG (or whatever you're used to).
That's the second time you've grossly misrepresented what's been said in laying out this thread. Keep it up and I might start thinking you're a troll. I see no assertion by Behe that multiple, simultaneous mutations are "required" for the "typical" evolutionary adaptation. Don't just make things up, address what's here.
Comment by Joy — August 20, 2008 @ 6:22 pm
August 20th, 2008 at 7:29 pm
Joy,
So, if the "edge" that he is probing is not relevant to "typical" evolutionary adaptation, of what significance is it? Behe makes it very clear in EoE that even the evolution of new protein-protein binding sites (which are required for the creation of molecular machines) is hampered by an asserted requirement for multiple, simultaneous mutations. Oh, so maybe not the "typical" adaptation, just all the really important ones.
Behe: "So it seems that the odds of development of a new, useful, specific, protein-protein interaction are less than one in 10^23—worse than a CCC." (p. 137)
What nonsense!
Here's more:
Behe: "No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past 10 million years" (p. 61)
No argument here, but why does he emphasize this point if he does not regard it as an impediment to evolution?
I couldn't make this garbage up if I tried.
Comment by David E Levin — August 20, 2008 @ 7:29 pm
August 20th, 2008 at 7:48 pm
David E Levin:
Yeah. We hear that a lot. What you're refusing to acknowledge is that Behe (and most folks here at TT) don't have a problem with evolution. Common ancestry, trial-and-error, enviro-system feedback loops, horizontal transfer, jumping genes, punk-eek and all.
What we've got a problem with is the wall around variation labeled "random." There's just too much evidence existent and incoming that things aren't "random" at all (though accidents happen - and disease results). In fact, things are looking positively front-loaded in these days of newer, better tools. If it's real science, you'll have this.
I don't have any problem at all looking at a trait and perceiving its survival/ecological value to all systems in the mix. I can also see the rationale behind change to meet challenge head-on. I just don't buy the pretense that it's all random apart from the "Wheel of Karma" aspects of natural constraints (selection).
I suspect life did in fact evolve to be what it is from common ancestors and experience of life on planet earth. I just don't buy your simplistic pablum as explaining what I see.
Comment by Joy — August 20, 2008 @ 7:48 pm
August 20th, 2008 at 7:55 pm
Joy,
How so?
Comment by David E Levin — August 20, 2008 @ 7:55 pm
August 20th, 2008 at 8:04 pm
Joy:
If you could clarify your problem a little. (1) What part of evolutionary theory relies on randomness according to you, and what's wrong with that? (2) What, exactly, is front-loading, and when and where has it ever been observed?
Comment by Raevmo — August 20, 2008 @ 8:04 pm
August 20th, 2008 at 9:21 pm
Hi DaveScot,
My my, Bilbo's thread has generated a lot of interest. Now that Joy has officially opened up the thread's scope of discussion, allow me to say I'm pleased you chose to join us.
You wrote…
I would agree that Mike Gene's The Design Matrix (only $16.47 at amazon.com) is an excellent book for not only ID critics but for ID proponents as well. I am glad that you have changed your opinion and applaud the public apology you offered Mike.
However, I disagree that the essence of Mike's book has anything to do with "The only reasonable explanation…" for either side. The main point of the book is how the same evidence can be reasonably seen as a duck (not designed) or a rabbit (designed).
There is no sharp "edge" between designed and not designed. It is a continuum where everthing can be seen as designed and not designed.
This is the point of both The Design Matrix the book and The Design Matrix the scoring system.
It is clear Mike made an honest and earnest attempt at investigating ID protoscience without attempting to force or spin a predetermined answer.
I haven't had a chance to get my hands on Genetic Entropy, but I have gone through The Edge of Evolution. Frankly, I think Darwin's Black Box was better because it was bolder. It came from a time when the ID Movement's leaders were willing to bet scientific vindication was just around the corner.
Are God and Chance the only two choices?
Your description of a problem with observation reminds my of something else that has a measurement problem, Quantum Mechanics.
Experimental evidence for Quantum Weirdness (i.e. EPR paradox) is the scientific observation of quantum interactions overcoming statistical constraints.
Behe has indicated many times that the closer one looks, the stronger the evidence for design becomes. Why did Behe stop at the cell level?
The only mention of Quantum Physics in Behe's The Edge of Evolution was a passing reference to Einstein.
Where are the ID explanations?
Where are the ID hypotheses?
Where is the ID Science?
The hypothesis of interconnected quantum effects is an ID alternative that could vindicate proponent’s trust.
Too bad this ID alternative is "…way down the totem pole" for some leaders of a certain political movement with religious goals Link
Comment by Thought Provoker — August 20, 2008 @ 9:21 pm
August 20th, 2008 at 10:14 pm
Presuming that it is still acceptable to post comments that relate to Bilbo's opening post, I am posting a link to a paper concerning details on how IMP-1 metallo-β-lactamases mutated into being imipenem resistant.
But before you jump to see the answers in the back of the book, think about what would help or hurt Behe's hypothesis as you understand it. Otherwise you might fall into the trap of declaring whatever the answer is as supporting the biased opinion (pro or con).
Think about the answer to these questions…
1) If it turned out that a single, highly improbable mutation was the cause, would it hurt or help your opinion?
2) If it turned out that multiple, reasonable mutations was the cause, how many mutations would it take to cross the hurt/help threshold of your opinion?
3) If it turned out that the outbreaks could be traced to a common ancestor, would it hurt or help your opinion?
4) If it turned out that several outbreaks were unrelated, how many unrelated outbreaks would it take to cross the hurt/help threshold of your opinion?
paper's link
Comment by Thought Provoker — August 20, 2008 @ 10:14 pm
August 21st, 2008 at 4:54 am
Hi TP. These are good questions:
I hope you realize they are also irrelevant to those critical of Behe unless the answers are perceived as discrediting Behe's position.
Comment by Bradford — August 21, 2008 @ 4:54 am
August 21st, 2008 at 10:35 am
Hi Bradford,
Once again you seem to be framing the discussions as the other side’s single-minded attacks of your side’s position. To turn your proclamation around, do these question become irrelevant to those supportive of Behe unless the answers are perceived as discrediting ID critics?
You did not offer your answers to the four questions. You did not give an indication of formulating your answers prior to looking at the results. You didn’t even indicate whether or not you looked at the results embodied in the link I provided. These questions are applicable for more than just “discrediting Behe's position”.
I am one of those people disinclined to presume Behe’s is automatically correct and subject his views to critical analyses. The original purpose of this thread was to critically analyze one specific excerpt from Behe’s Edge of Evolution. However, as Joy pointed out, we are capable of expanding the discussion beyond that. I happen to think the questions I asked are applicable to the hypothesis that evolution might be affect by interconnected quantum effects. The evidence surrounding the acquisition of imipenem resistance in nature but not the lab would be part of a “consilience of clues” for a third choice hypothesis that isn’t dependent on a presumption of the either randomness or God existing.
Comment by Thought Provoker — August 21, 2008 @ 10:35 am
August 21st, 2008 at 10:55 am
ThoughtProvoker
If you expect problems in quantum physics to be explained by intelligent design proponents then it's only fair to expect the same of proponents of the modern synthesis. I fail to see how the scope of either encompasses the generation of fundamental theories in physics. Please explain.
In the meantime, the lack of a quantum gravity theory notwithstanding, statistical mechanics has been immenently successful in predicting the behavior of matter in bulk quantities where chemistry is applicable. Last I knew the current thinking by a majority is that biology is explained by chemistry and chemistry is explained by physics. I happen to agree with that hierarchy.
The science behind ID lies in physics, particularly in statistical mechanics.
Comment by DaveScot — August 21, 2008 @ 10:55 am
August 21st, 2008 at 10:57 am
You're right. I did not answer the questions but don't expect critics to either. As for Behe's position, as an IDist, it does not concern me as much as it does the critics what Behe believes. He is one of many fish in the pond whose primary claim to fame is his notoriety as an author. Nothing wrong with that but it is typical of your side's movement to focus on Behe and Dembski as if to think that discrediting them discredits a more encompassing idea that is larger than both. When I look at the comments in this thread one theme stands out- Evolution dunnit. I don't want to hear about impediments. I might be tempted to believe this belief is based on an objective assessment of the evidence. Except for one thing. When there is a distinct lack of evidence they still believe. That's why I repeatedly raise the origins issue. It's a reminder that there are two movements.
Comment by Bradford — August 21, 2008 @ 10:57 am
August 21st, 2008 at 11:04 am
Getting back to Bilbo's question, Matzke's initial post was correct in that there are other possible mechanisms aside from the evolution of one single enzyme that can explain increased antibiotic resistance in this case. Until we know precisely what molecular changes are responsible for the evolution of increased resistance we can't say whether or not Behe's hypothetical boundary has been exceeded or not.
Comment by DaveScot — August 21, 2008 @ 11:04 am
August 21st, 2008 at 12:02 pm
I think it was Bilbo who focused a thread on "Behe's Test".
Comment by Zachriel — August 21, 2008 @ 12:02 pm
August 21st, 2008 at 12:35 pm
Bilbo wrote the blog entry. If the name had been John Smith, an unknown researcher who made the following ID claims, the responses would have been few in number.
Comment by Bradford — August 21, 2008 @ 12:35 pm
August 21st, 2008 at 4:14 pm
Raevmo asks:
The arch-proponent of "front loading" was generally accepted to be associate Professor (retired) John Davison until DaveScot pointed out that he had arrived at the same idea independently. As DaveScot is posting here at TT, for the moment at least, perhaps he can enlighten you.
Comment by Alan Fox — August 21, 2008 @ 4:14 pm
August 21st, 2008 at 4:50 pm
Sorry, I forgot to provide the link (You need to scroll down to the appropriate comment)
Comment by Alan Fox — August 21, 2008 @ 4:50 pm
August 21st, 2008 at 4:50 pm
Hi DaveScot,
You wrote…
Maybe you missed that I AM the "intelligent design proponent" offering up a design hypothesis wrapped around bioquantum physics as seen by Sir Roger Penrose and Dr. Hameroff.
This is the result of being open minded enough to look past my general distrust of the ID Movement to listen to ID proponents like TT's Joy.
Here is a link to The Magic of Intelligent Design and The Third Choice.
I have argued this hypothesis both here and at After the Bar Closes. I would also argue it at Uncommon Descent but… well… here is the link to where you disinvited me.
I'm past due for an update. I am waiting for a break in my work schedule to offer a Guest Post.
Comment by Thought Provoker — August 21, 2008 @ 4:50 pm
August 21st, 2008 at 5:04 pm
I'm having problems with the spam filter again.
There is a comment stuck that points out that I have been a design proponent arguing a hypotheses suggesting interconnected quantum effects could cause design in living organisms.
Comment by Thought Provoker — August 21, 2008 @ 5:04 pm
August 21st, 2008 at 5:14 pm
Wouldn't you be better taking your ideas to your own blog like Mike Gene has done?
Comment by Alan Fox — August 21, 2008 @ 5:14 pm
August 21st, 2008 at 6:31 pm
Hi Alan,
You asked…
Sure, but then I would have to admit I'm serious about this.
If you click on my name, it will take you to my blog (such as it is).
Comment by Thought Provoker — August 21, 2008 @ 6:31 pm