An Open Letter to Dr. Michael Behe

| 41 Comments

Dear Dr. Behe

I have recently read your response to Abbie Smith’s article on the HIV-1 protein VPU. Ms Smith showed how Vpu’s recently evolved viroporin activity directly contradicts your statement that HIV has evolved no new biding sites since it entered humans (Edge of Evolution, page 143 and figure 7.4, page 144 ). I was greatly disappointed in your response. I must admit to having a special involvement in this case. Firstly, I drew the illustrations for Ms Smith’s article, and its follow up. But secondly, as a member of my professional association’s education committee, I am directly concerned with the support and nurturing of the new generations of enquiring minds, those that we will pass the torch of enquiry on to when we retire. It is in this regard that your response very disturbing. It is almost the exact opposite of what a concerned scientist and science communicator should have done.

It was bad enough that you chose to ignore her for over two months and then did not do her the courtesy of replying on her blog (1). It was bad enough that you chose to start by belittling her and playing the “I’m a Professor and she is a mere student” card (conveniently ignoring the fact that she actually works on HIV). This is particularly egregious in science, where we pay attention to the evidence and logic of an argument, rather than the letters after an author’s name. Doubly so if we wish to guide young scientists into a demanding profession.

But by far the worst, you ignored her core argument. That in the space of a decade HIV-1 Vpu developed a series of binding sites that made it a viroporin, a multisubunit structure with a function previously absent from HIV-1. Dr. Behe, it is not enough to cite a generalist review and claim that the differences between HIV-1 strains are “not all that great”. You actually have to show why Vpu developing binding sites to form a multi-subunit structure with a novel function does not falsify your claim that HIV has developed no new binding sites. Ironically, the very paper you cite to dismiss Ms Smith contains evidence of at least two new binding sites in HIV. I will not dwell on this any further, as Ms Smith is producing her own response.

Viroporin.jpg

Diagramatic representation of a viral viroporin (ion channel), such as Vpu. SIV Vpu and non-M class HIV Vpu’s do not have viroporin activity. This is exactly an example of the kind of protein-protein interaction and new molecular machinery that Dr. Behe demands, but has completely ignored in his response to Ms Smith. Image from FEBS Letters 552 (2003) 28-34.

But I will comment on one other aspect of your response. Not content with dismissing Ms Smith, you make an incorrect statement as a central part of your argument.

Another, more important point to note is that I’m considering just cellular proteins binding to other cellular proteins, not to foreign proteins. Foreign proteins injected into a cell by an invading virus or bacterium make up a different category. [emphasis added here[by MB]] The foreign proteins of pathogens almost always are intended to cripple a cell in any way possible. Since there are so many more ways to break a machine than to improve it, this is the kind of task at which Darwinism excels. Like throwing a wad of chewing gum into a finely tuned machine, it’s relatively easy to clog a system — much easier than making the system in the first place. Destructive protein-protein binding is much easier to achieve by chance.

This is simply not true, either generally (2) or in the particular case of Vpu. Importantly, your statement shows that you do not understand what Vpu does. Vpu down regulates the surface protein CD4 (the Viroporin activity is something separate related to viral release). It does not “gum-up” CD4, it specifically binds to it, then binds to a separate protein (the βTrCP subunit of the SCFβTrCP ubiquitin ligase complex) in the Golgi apparatus (all except the C strains, which target the plasma membrane). This multiprotein complex links to the ubiquitin-proteasome pathway, where CD4 is ignominiously broken down by the cells own mechanisms. This CD4–Vpu–βTrCP complex is NOT mere “gumming up of the works” but a precise targeting of CD4 the proteosome by Vpu. This is not obscure, but has been well known for some time.

Vpu_binding.jpg

Vpu binding to CD4 and βTrCP, which then targets CD4 for degradation. As you can see this is not Vpu randomly gumming up the works, but a macromolecular complex of the sort Behe demands. Taken from Margottin F, et al., 1998

In the context of Ms Smith’s argument, HIV-1 Vpu has a new binding site, YRKL in the cytoplasmic alpha helical section, not present in SIVcpz Vpu, which efficiently targets Vpu to the Gogli complex, making the degradation process more efficient. Can you please explain why the appearance of a new targeting motif in HIV-1 Vpu is NOT an example of a new binding site.

The fact that you chose to dismiss Ms Smith on the basis of your ignorance of how Vpu actually works, as well as ignoring her central argument is of great concern. As scientists, we have a duty both to deal with arguments carefully, and to nurture upcoming young researchers. Dr. Behe, you have failed both these duties. You owe Ms Smith a complete apology for such behaviour.

Your sincerely, Ian Musgrave

(1) Unfortunately, I can’t reply on the Amazon blog, as Amazon does not remember my purchases there, perhaps some kind soul will repost my letter there.

(2) As a rule neuroscientists and molecular biologists get excited over toxins because they are so specific, not because they general gunge up things. However, this is not the place to discuss injectable toxins.

References:

Margottin F, et al., A novel human WD protein, h-beta TrCp, that interacts with HIV-1 Vpu connects CD4 to the ER degradation pathway through an F-box motif. Mol Cell. 1998 Mar;1(4):565-74.

Bell CM, et al., Molecular Characterization of the HIV Type 1 Subtype C Accessory Genes vif, vpr, and vpu. AIDS Research and Human Retroviruses. 2007, 23(2): 322-330.

Musgrave IF, Seifert R, Schultz G. Maitotoxin activates cation channels distinct from the receptor-activated non-selective cation channels of HL-60 cells. Biochem J. 1994 Jul 15;301 ( Pt 2):437-41.

41 Comments

Methinks Dr. Behe had to dismiss ERV’s arguments because he cannot face them. She appears to have directly falsified his core argument about HIV, and thus, by extension, pretty much the whole of The Edge of Evolution. (I mean that, since he was so egregiously wrong about HIV, what is to reassure us that he may be right about anything else, such as Plasmodium?).

Of course, I expect the IDC crowd will now claim the new binding sites of Vpu as evidence of design.

I posted it on Amazon, along with the link. (I did remove the image captions, because they didn’t make sense without the images.)

It appears that Behe can’t deal with being pwnd by a girl (to the civilized, a young woman). What a creep.

I can’t wait to see how will dr. Behe mangle his response this time. Can he really weasel his way out? He probably can with the ID crowd, but the real scientists? No way, that is precisely the reason why scientists are rather unimpressed with his results, if you can call them that.

I like the way Abbie refers to him as mr behe, rather than dr behe - that is probably the biggest insult to him but then again he is wilfully choosing to ignore his training in defence of his position so maybe his title should be rescinded? It’s unfortunate that the general public rarely make the connection that holding a PhD doesn’t preclude you from being a moron! Sadly, he will always find an audience.

Toni Petrina asks, “Can Behe really weasel his way out?”

The more important question is, WHY is he weaseling?

Scientists make mistakes all the time. They innocently make errors in logic, use contaminated chemicals, etc. And then– they admit their mistakes, issue retractions if necessary, pick themselves up and go on.

If scientists are attacked in ways that they consider unfair, they may point out misunderstandings, errors in their critics’ logic, or possible contaminants in their critics’ experimental results.

They do NOT (if they want to remain productive members of the scientific community) weasel. They do not launch ad hominum attacks or muddy the waters with waffling redefinitions that contradict their own original statements.

Michael Behe must surely know all that. He must surely know that the scientific community will consider his response yet more proof that as a scientist he is a flagrant fraud. So who is his real audience? The Disco Institute? Wealthy Christian dominionists? The public who buy his books in the forlorn hope he can prove science supports biblical literalism?

Because whoever he’s weaseling to try to impress, it’s not the scientific community.

Excellent post. Obviously, we’ll all be waiting for Dr. Behe’s response. A fun idea would be to have Dr. Behe present a talk at OU to address these issues. Of course, a question and answer period at the end would clear up any confusion in the audience. I’m sure we could find some sponsors. Actually, I’d pay good money for that ticket. DG

We should also note ERV’s other followups:

Although she calls herself a “pre-grad student,” the tone of the post is decidedly junior high, the tone of someone who is trying hard to compete with all the other Mean Girls on that unpleasant website. I’ll pass over all that and try to stick to the substance.

Michael Behe– I have never encountered scientific sexism until right now.

He isn’t pubjacking! He’s commandeering a publication!

No, this is not my official ‘response’ to Behe. But I thought this was significant enough for its own post. The second prophesy has been fulfilled!

So whos the author of the pubjacked lucky paper? Cristian Apetrei of Tulane, and his article “HIV Genetic Diversity: Biological and Public Health Consequences” :

Butler at al (HIV Genetic Diversity: Biological and Public Health Consequences, Current HIV Research, 2007, 23-45) remark under the subheading “Biological Consquences of HIV Diversity”:

With such breadth of genetic diversity among HIVs, one might expect significant biological differences between the clades. Although interesting variations can be seen, much of the data concerning biological implications of HIV diversity is contradictory.

Plenty of differences do exist, and some are “interesting”, but not all that great.

Hmmm. Now that statement looks funny. I mean it lacks the tell-tale “…” that usually mark Creationist quote-mines, but something just looks fishy about Behes choice of quote. Hmmm. Wonder what comes right after the portion Behe chose to quote?

The long terminal repeat region (LTR) of the HIV genome regulates transcription and viral replication, acting as a promoter responsive to the viral Tat protein. Although all subtypes share the same LTR function, they differ with respect to LTR sequence structure, basal activity and response to cytokines and transcription factors [95]. The majority of HIV-1 group M subtypes contain two nuclear factor binding sites (NF-kB). A minority of subtype C contain an extra NF-kB that may promote replication in the presence of TNF-and chronic immune activation [135]. CRF01_AE, in contrast, has one NF-kB site, but contains a different transcription factor binding site that may allow it to replicate in a wide variety of cells. Indeed, when compared with other subtypes, CRF01_AE encodes a highly potent LTR region [2, 135, 257]. Although there are clear differences in LTR sequences and basal replication capacity among subtypes, the influence of these molecular level changes on specific subtype epidemics and the global spread of the virus remain uncertain.

You know, that kinda looks like my essay, except looking at LTRs instead of Vpu. And they dont stop with one example! They go on to describe several more genetic differences between HIV-1 subtypes and what researchers think those differences mean biochemically… but like a true Creationist, Behe ignores all of that information and attaches his suckers to the fact that the authors admit “We dont know everything.”

ERV takes no prisoners!

Can you send an open letter to a closed mind? Just asking…

Behe is writing for the public, and so I doubt that he cares very much about these specific refutations that are so difficult for the public to understand.

No doubt you are correct in everything you say, and yet I must admit that as a typically ignorant member of society, I have no idea why. In fact, I have very little idea as to what you said. Of course, you are not really writing here for the general public and have no obligation to do so, but for whatever it’s worth (if anything), here’s what your article sounds like to one of the ignorant:

I can follow Behe, as he appears to say that Smith’s work doesn’t contradict his comments because her work is about some outside “thing” that attacks and damages cells while his own earlier comments, he claims, referred to the natural functioning of undamaged cells. He didn’t say the foreign protein actually “gums up” the cells, just that the foreign protein sorts of breaks the cell in the same random way that gum tossed into a delicate machine breaks it. So, he’s saying, if a random toss of foreign matter into a machine can do harm, it isn’t surprising that Smith shows that cells can be damaged by chance. They just can’t be made to function better by chance.

As far as I can tell, you agree that her work concerns a foreign thing that enters the cell and results in damage.

Vpu down regulates the surface protein CD4 (the Viroporin activity is something separate related to viral release). It does not “gum-up” CD4, it specifically binds to it, then binds to a separate protein (the βTrCP subunit of the SCFβTrCP ubiquitin ligase complex) in the Golgi apparatus (all except the C strains, which target the plasma membrane). This multiprotein complex links to the ubiquitin-proteasome pathway, where CD4 is by the cells own mechanisms. This CD4–Vpu–βTrCP complex is NOT mere “gumming up of the works” but a precise targeting of CD4 the proteosome by Vpu.

Out of this, I can make out that Vpu is maybe the name of the outside thing that does damage? It binds to “the surface protein CD4” (which is maybe the original thing that eventually gets damaged?), with “binds to” still sounding an awful lot like what happens when gum sticks to a machine part. The next piece of your comment that makes sense to me is “ignominiously broken down,” which sounds a lot like Behe’s “cripple a cell in any way possible.” You then say “NOT mere ‘gumming up of the works’ but a precise targeting,” which seems to say that Behe’s wad of gum sticks to some part of the cell machine, but not to others, and causes a specific disturbance, not a vague one. But it is indeed, according to your sentence, a “gumming up of the works,” just not a “mere” gumming up.

So, OK, the entry of the foreign object doesn’t cause damage in some unspecified way; it attaches to something specific, which causes a specific series of events, resulting in a specific problem, none of which I understand, though I grant it’s very important.

But how does any of that contradict Behe? He said (I think??)that he was claiming no evolved changes to the normal process as that’s too complicated for random evolution, though we can expect chance events to account for damage. I do understand (I think??) that evolution itself isn’t really random (because of natural selection), but I still can’t make out how Smith’s work actually contradicts Behe’s claim as she seems to be just showing the details of the throw-the-foreign-element-in-to-mess-up-the-works process.

George Smiley Wrote:

t appears that Behe can’t deal with being pwnd by a girl

Are cooties intelligently designed?

JuliaL - interesting questions and others will no doubt be able to answer them more fully.…But I can at least say that Behe was wrong to talk about the viral protein somehow breaking or disrupting the cell. Rather, the virus wants to the cell to keep running so that the cell can be hijacked by the virus to make more viruses. It is usually true that the cell will eventually die as a result, but this is definitely a case of functional interaction rather than a mere case of “throwing in a monkey wrench” to kill the cell.

Mike Z,

Oh … Already, much clearer! Thanks.

hoary puccoon Wrote:

So who is his real audience? The Disco Institute? Wealthy Christian dominionists? The public who buy his books in the forlorn hope he can prove science supports biblical literalism?

Much more than that. Add the majority that hates science and loves anything alternative. One that learns evolution not in science class, but through feel-good sound bites from a sensationalist media. One that is mostly not Biblical literalists, but nevertheless still says “it’s only fair to teach both sides,” and “I hear that the jury’s still out about evolution.” With that big an audience, what does he care what scientists think of him?

BTW, after 11 years has anyone heard if Behe apologized for inserting a period in a sentence in a paper by Coyne and Orr?”

Regarding the question of how Behe would weasel out of the unenviable position Dr. Musgrave’s post put him in, Behe has several options. One, used by him more than once before, would be to pretend Dr. Musgrave does not exist. That is what happened when I posted online (in 1999) and later published in print (2003) an article critical of Behe’s egregious misunderstanding of probabilities and complexity (being not a biologist, I abstained from discussing the biochemical aspects of his output). My article was translated into other languages, reviewed repeatedly, and initiated an online debate. Behe’s reaction? Dead silence. Perhaps this was the best answer that could be expected: Behe’s silence, beyond doubt, had a simple reason - he just could not come up with any reasonable counter-arguments. So he chose to pretend I do not exist. Such a behavior, coupled with his supercilious ad-hominem remark addressing Abbie, and with his spectacular fiasco at the Dover trial, allows one to list Behe in the same category as Dembski -that of pseudo-scientists.

Frank J - Thanks for the link! I have saved the article to my hard drive as “Behe Quote Mine”.

Hey FTK - are you paying attention?

Hi, I’m only just starting my undergraduate biology degree, and my knowledge of biochemistry and molecular biology is still very skim, I just wanted to ask Ian just one thing, and I’d like it explained in layman’s terms, even though I do have SOME background in biology -

How do we know (or why are we fairly certain) that HIV evolved from SIV or that the type with the new binding sights evolved after the version of it without? How do we know it’s not the other way around?

I’m probably displaying huge ignorance here, which I admit - but asking questions is usually how we remove ignorance.

Thanks Ian for the wonderful post.

J-Dog Wrote:

Thanks for the link! I have saved the article to my hard drive as “Behe Quote Mine”.

Better make that “Behe Quote Mine No. 1,” as you will surely find many more.

Sickle cell,

When we take the sequences of SIV and HIV strains and build a “relatedness” tree from them, what you see is that HIV emerges from the SIV grouping in the tree. It happens just like how the “sun bear” emerges from the bear grouping in this tree.

@JuliaL

Basically what Behe is saying is that these sorts of things are like throwing a wrench in a machine (he uses gum but a wrench is a bit clearer). It just sort of breaks whatever it comes in contact with. It doesn’t matter what type of component it messes up, it could be a gear, a pulley, a belt, an electrical contact. Nor does it matter which specific ones of these it messes up. Whatever the wrench messes up will break the system. If you look back after the system has broken you can see that a specific damaged component led to the breakdown, but there is no reason the wrench had to damage that specific component. Any damage would have worked.

VPU, however, does not operate like this. You cannot just toss it into a biochemical system and have whatever component it comes in contact with break down. It is extremely specific. It would be more like a very carefully sized and shaped gear that, when added to the system in a very specific site and in a very specific manner in a very specific orientation, will cause part of the machine to start doing something fully functional but very different than what it was originally doing. It does this by causing part of the machine to disconnect itself from the rest of the machine. The gear doesn’t do the disconnecting or the breaking, rather it alters the machine in such a way that that machine does this itself. And this disconnected component is a component that is detrimental to the functioning of the virus.

The similarities to an intelligently-designed system in the case of VPU is striking, so much that it is precisely the sort of thing Behe said could not evolve. The problem is that it did evolve. Behe, of course, is trying to downplay this any way he possibly can. He does so by grossly mischaracterizing what VPU does. He portrays it like I did in my first paragraph when it really behaves in a manner much closer to my second paragraph. The problem is that not only is his entire argument based on the assumption that this sort of thing cannot evolve, his entire worldview is based on that assumption. So instead of operating like a real scientist he insults the person who pointed out the issue and then makes up a strawman (i.e. imaginary) version of the system and then argues that this strawman does not contradict his position.

He crafts his arguments, as you have noticed, in such a way that is convincing to people who do not understand biochemistry or do not understand creationist tactics because that is the audience he is trying to convince. He knows very well that he will never convince the scientific community because they know better. The only reason he even addressed VPU is because it is something that non-scientists can understand (“Behe said HIV has not evolved this biochemical thingamajig but it has”). All he has to do is make a counterargument that would convince this sort of audience. Once that is accomplished it gets into the minutia of the arguments and peoples’ eyes start glazing over. Now that he has done this I doubt we will hear much, if anything, about this issue again from him, just as he has done with his previous arguments that were demolished.

Sorry, but I have to agree with Behe that the tone of Ms Smith’s post is junior highish. Why not stick to the factual arguments without trying to be cute, funny, insulting, etc? Besides, after having had every invective in the book thrown at him by Mark Chu-Carroll, Behe is probably quite hardened by now.

Sorry, but I have to agree with Behe that the tone of Ms Smith’s post is junior highish. Why not stick to the factual arguments without trying to be cute, funny, insulting, etc? Besides, after having had every invective in the book thrown at him by Mark Chu-Carroll, Behe is probably quite hardened by now.

I assure you, sir, my monocle literally popped from my face in shock at Madame Smith’s impertinence.

Sorry, but I have to agree with the scholars on this site that Behe’s argument was effectively demolished by a senior student.

Sorry, but I have to point out that senior students, like ERV, are at the very top of their game in terms of scholarship, a game from which Behe withdrew decades ago.

Sorry, but I am at a loss to explain why Behe did not stick to the factual arguments, rather he tried to be cute, funny and insulting.

Sorry, my mistake; Behe doesn’t have any factual arguments.

Julial wrote:

I can follow Behe, as he appears to say that Smith’s work doesn’t contradict his comments because her work is about some outside “thing” that attacks and damages cells while his own earlier comments, he claims, referred to the natural functioning of undamaged cells.

This is Behe’s first piece of misdirection. Ms Smith’s article was about Vpu protein-Vpu protein interactions that form a novel functional structure, an ion channel (viroporin), exactly the thing Behe demands, not external proteins “damaging” the cells. The main takehome point is that Behe did not reply to Ms Smiths evidence.

Out of this, I can make out that Vpu is maybe the name of the outside thing that does damage? It binds to “the surface protein CD4” (which is maybe the original thing that eventually gets damaged?), with “binds to” still sounding an awful lot like what happens when gum sticks to a machine part.

Binding is the generic term for proteins interacting with other proteins. Here Behe misdirects again, by claiming this isn’t the kind of specific binding he is talking about that builds molecular machines. But in fact it is precisely the kind of specific binding he wants, and makes a mini “molecular machine” (that the molecular machine breaks down one protein is irrelevant, as this kind of cellular “garbage disposal” is one of the sorts of molecular machine” that Behe describes.

So that is two strikes against Behe, he ignores the actual argument, and completely misunderstands the straw argument he uses instead.

Coin: That’s weird. Why was there a monocle in your face?

Doc Bill: You have nothing to apologize for. I did because I ventured into a (very mild) criticism of the tone of Ms Smith’s piece. With her strong arguments, that was unnecessary and made for a less interesting read. C’est tout.

Thank you very much, Ian! And thanks to the rest of you for your support :)

What I love about this exchange is that it provides us the opportunity to compare/contrast what each of the “leading ID scientists” have to say about their own game.

Behe: “So what? You have a mutation by mutation account? Pfff. Thats not so great.”

Dembski: “I need to see mutation by mutation accounts of evolutionary pathways!”

Heads ID wins, tails evolution loses.

I’m not a scientist any more than JuliaL, but from my limited knowledge of biology, Behe’s argument seems fishy from square one. He writes that the proteins of pathogens “almost always are intended to cripple a cell in any way possible.”

Huh? Why are pathogens doing that? It’s my understanding that viruses and other pathogens are parasites using our cells as a vehicle to pass on their own genes. “Crippling a cell in any way possible” might make sense if pathogens were designed by an Intelligent (but really Nasty) Designer to make our lives miserable. But if the pathogens are just trying to survive and reproduce, why would they bother gumming up our works, instead of coopting our cells for their own uses? How would that help them avoid extinction? It would be like Iowa Beef Packers machine-gunning a herd of cattle. Sure, it would kill a lot of cattle in a hurry– but it wouldn’t produce any steaks, and it wouldn’t help IBP stay in business.

Either I am way off base, or Behe isn’t even trying to make a logical argument here. He’s pushing emotional buttons in people who aren’t scientists and who, he’s betting, will be impressed enough by his credentials and his jargon not to think to closely about what he’s saying.

I really appreciate the efforts to clarify for me, and I think I have the essence of it now. It isn’t true that evolution here has resulted in nothing but a loss; a new function has actually evolved, exactly what the ID people say can’t happen.

TheBlackCat,

All he has to do is make a counterargument that would convince this sort of audience. Once that is accomplished it gets into the minutia of the arguments and peoples’ eyes start glazing over.

You’re quite right. I’m not much of an eye-glazer when it comes to complexities that I can actually work out; like many other people who know little about science, I’m willing to put in the effort to think. But when it just isn’t possible to follow the technical argument because of ignorance about the meanings of the language involved, eye-glazing is the result, just as you say. Though I did read Smith’s linked post and re-read this one a number of times, I was quite lost. I just didn’t grasp that a new function had developed. Also, in this case Behe seems to have been misleading about what the issue is. He certainly seemed to saying that nothing happened other than damage. This is an ID claim I’ve read many times in one form or another: evolution can damage, degrade, or lose functions but it can never add anything useful and new.

Ian Musgrove,

Ms Smith’s article was about Vpu protein-Vpu protein interactions that form a novel functional structure, an ion channel (viroporin), exactly the thing Behe demands, not external proteins “damaging” the cells.

Wonderfully clear. As I assume you are the same person Smith refers to, I thank you for taking the time from your work to respond to my confusion.

I think perhaps the single greatest strength of the ID people is not that they appeal to fundamentalist religious notions: that’s their second greatest strength. The greatest is that they say (apparently mostly untrue) things in a way the rest of us can actually understand. Communication with the general public is not a strong point for the scientific world. I know most scientists are too busy for that, but maybe it would be good if more scientific people more often added brief statements of the significance of their material, phrased in very simple terms. No, I’m not suggesting that Panda’s Thumb posts ought to be oriented to people as ignorant as I am - just that the occasional little simply-phrased hint is awfully helpful and very welcome.

hoary puccoon:

Toni Petrina asks, “Can Behe really weasel his way out?”

The more important question is, WHY is he weaseling?

Scientists make mistakes all the time. They innocently make errors in logic, use contaminated chemicals, etc. And then– they admit their mistakes, issue retractions if necessary, pick themselves up and go on.

If scientists are attacked in ways that they consider unfair, they may point out misunderstandings, errors in their critics’ logic, or possible contaminants in their critics’ experimental results.

They do NOT (if they want to remain productive members of the scientific community) weasel. They do not launch ad hominum attacks or muddy the waters with waffling redefinitions that contradict their own original statements.

Michael Behe must surely know all that. He must surely know that the scientific community will consider his response yet more proof that as a scientist he is a flagrant fraud. So who is his real audience? The Disco Institute? Wealthy Christian dominionists? The public who buy his books in the forlorn hope he can prove science supports biblical literalism?

Because whoever he’s weaseling to try to impress, it’s not the scientific community.

Check out the creationist FtK at After the Bar Closes. You’ll see that Behe succeeds with his target audience.

JuliaL– We got you covered!

Quick translation for laymen

Illustrated guide to VPU

I really, really want everyone to be able to understand this :) Its friggen cool :)

Goddammit.

Right link to ‘Quick Translation.’

ERV Wrote:

JuliaL– We got you covered!

Quick translation for laymen

Illustrated guide to VPU

I really, really want everyone to be able to understand this :) Its friggen cool :)

[tongue-in-cheek]Thanks for the links, but I was a bit puzzled about the phylogeny: are you saying that HIV is related to monkeys and chimpanzees, or that HIV is related to viruses that infect monkeys and chimpanzees??[/tongue-in-cheek]

Here’s an interesting HIV/evolution paper just published online at PNAS. It’s free access too:

Variation in HIV-1 set-point viral load: Epidemiological analysis and an evolutionary hypothesis.

http://www.pnas.org/cgi/reprint/0708559104v1

Why not stick to the factual arguments without trying to be cute, funny, insulting, etc?

because Behe has been arguing well outside the usual bounds of acceptable behaviour for some time, and for academics who spend a lot of time having real arguments that resolve things, this is considered not just irritating, but insulting. In the case of ERV, Behe has been mainly using “argument by harumph”. I am really pleased to see that the attack dogs are putting him to the rack - refusing to let up until he makes an acceptable account of himself. And this process has a large sociological component - basically making it abundantly and vigorously clear where the evasions and ludicrous arguments are, and that they will not be tolerated. The approach of just writing technical rebuttals and not doing anything the ID faction will consider rude allows plenty of wiggle room for Behe to bleat away triumphantly without tackling the points his opposition makes. And in public lectures, if Behe speaks without hecklers from the floor holding him to the flames, he will do more of the same. Behe

Coyne and Orr had the measure of Behe’s irreducible crankiness 10 years ago, TheBlackCat pounces on the same non-flying bird, and Behe himself puts in an effort to show us exactly what his tricks are.

The next time I see someone refer to Behe as a kind enough man in person I will know the score.

From a layman’s perspective:

Behe:

Since there are so many more ways to break a machine than to improve it, this is the kind of task at which Darwinism excels. Like throwing a wad of chewing gum into a finely tuned machine, it’s relatively easy to clog a system — much easier than making the system in the first place. Destructive protein-protein binding is much easier to achieve by chance.

This is exactly the same language as what annoyed me so much when I first read “Darwin’s Black Box” 10 years ago: Behe is on a propaganda mission! I suppose mouse traps and ‘wads of chewing gum’ go down well with his captive audience, but to a free thinking individual it is a clear giveaway.

Coin: That’s weird. Why was there a monocle in your face?

It had been stuck there since the Accident.

ERV wrote:

Thank you very much, Ian! And thanks to the rest of you for your support :)

Yesterday I was involved in our Faculties research expo. Here we showcased the ongoing research of our PhD students. Apart from the high quality of the research involved, I was impressed by the commitment of the academics to support and mentor students. The Dean made the same point I did about passing on the torch of enquiry. I think it is sad the Behe does not have the same collegial spirit, and the same understanding of our roles as mentors.

Ian– Thats definitely a point I want to get across to laymen, too. I am respectfully insolent (hehehehe) to my professors, my research mentor, my committee members, etc. “But that experiment would be pointless because…” “Yes you CAN make that inference from the data!” “Why you would suggest doing X when I already have Y optimized?”

It gets heated sometimes, but no one has ever been condescending. No one laughs off my statements with references to teen movies. No one backs away from my questions by fumbling basic science (‘39% AA similarity means its the same protein!’) or simply ignoring my Q.

I challenge them, I learn. They challenge me, I learn.

Ive learned nothing from Behe. His behavior is uncharacteristic of professional scientists, and revolting.

Sometimes you can determine what profession a person is in by who signs his/her paychecque.

By my account, that makes Behe a professional apologist, PR agent and fiction author.

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This page contains a single entry by Ian Musgrave published on October 22, 2007 5:44 AM.

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