An Open Letter to Dr. Michael Behe (Part 4)

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Dear Dr. Behe

I’m sorry you couldn’t follow Ms Smith’s argument. I found it quite easy, an elegant detective story that built up its case clue by clue. However, even if you couldn’t follow it, the viroporin story was pretty hard to miss. That Vpu evolved over the space of a decade, when viral numbers were low, into a viroporin, a multisubunit structure with a function previously absent from HIV-1, was an obvious key challenge to your assertions.

I’m sorry that you didn’t understand the context of her evidence about Vpu variability. The fact that Vpu has undergone more sequence change than the envelop proteins, which have a high rate of evolution as they evade the bodies anti-vital defences, is a clue that they are evolving. What kind of evolution? This segued into her evidence about the function of Vpu, which arose recently in chimpanzees (see the diagram at the bottom of this post, which shows where Vpu arose), using this as a stepping stone to Vpu becoming a Viroporin in HIV-1 M.

Yes, you did state that you specifically excluded viral host-protein interactions (except when you can’t find any examples of such interactions, then, in the example of viral protein binding to host cell receptors, you claim the absence of new receptor binding supports your position, pity about the evolution of CXCR4 co-receptor binding then). I’m sorry, such handwaving doesn’t help you.

Firstly, Vpu viroproin is an example of viral protein-viral protein interaction. Secondly, as I show in the post to which you are supposed to be responding, the claim that viral protein –host protein interactions just “gum up the works” is nonsense. We are talking about a coordinated binding to a specific acceptor site (in what possible way is the development of binding of viral gp120 to CD4 in any way different to binding of class II MHC to CD4, they even use much the same binding residues (Wang 2002)). This is exactly the kind of binding site interaction that you claim can’t develop (or rather is incredibly improbable to develop).

Thirdly, your claims about the difficulty of developing binding sites rests almost entirely on the difficulty of getting multiple simultaneous mutations, the down stream effects of a new binding site are irrelevant to your argument . But even so, when we talk about Vpu binding we are talking about a coordinated binding to a specific acceptor site. In the context of the Vpu function, this is the production of a multi-subunit molecular machine that sends CD4 to be broken down. The recently evolved Vpu binding sites change the targeting of this complex, with beneficial effects for the virus.


Vpu, no, it doesn’t “gum up the works”

You use a similar non-sequitur when it comes to the development of the casein kinase binding sites. You claim they are too simple, but your own example of a binding site is the haemoglobin S mutation, a single binding site. Your book categorically states no new binding sites in HIV, contrasting this with the one HbS one amino acid binding site mutation. At the very least, in the interests of honesty, in your book you should have noted the casein kinase binding sites and stated they were “too simple” for you (even though they require more than a single point mutation, which is where you claim things ramp up in difficulty, and they are more complex than your HbS example).

The casein kinase data should give you pause anyway. These are key, regulatory protein-protein binding sites. Activation and regulation of diverse proteins are dependent on these regulatory binding sites, and you claim they can develop easily. Yet they are no different to any other protein-protein binding site, and have a quite nice affinity for their enzyme. Might not the casein kinase site be a paradigm of how protein-protein binding develops, via multiple paths and through selectable intermediates? I would suggest reading Wang (2002) again, and paying particular attention to the role of amino acid F43 in binding to CD4.

Still, you admit you did see the viroporin section. This is a direct challenge to the very heart of your argument. Why did you ignore it?

Yours sincerely
A male featherless biped named Ian Musgrave

Wang J. (2002) Protein recognition by cell surface receptors: physiological receptors versus virus interactions. Trends Biochem Sci. Mar;27(3):122-6.

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Dear Gentle Readers: At the bottom of this essay, I’m collecting links to reviews of Behe’s book The Edge of Evolution, replies to reviews and so forth. Well, now the burden is off me, and I can devote my book-reviewing time to good books,... Read More


Is that a rhetorical question at the very end? He knows that he can’t deliver, he is simply buying credibility among ID/creationist folks by mere talking about this.

Is that a rhetorical question at the very end? He knows that he can’t deliver, he is simply buying credibility among ID/creationist folks by mere talking about this.

Why did you ignore it?

Cuz he doesn’t really give a hoot. In fact he’s probably enjoying all the attention. (Sorry to hear about the feathers, by the way.)

Mikey’s back–and this time it’s personal!

I wonder how Behe liked his re-enacted portrayal on Judgment Day? Based on his blog I would guess it went right to his head–Time magazine will just have to make him man of the year.

Ya all know, of course, that “Judgment Day” will rally the “real” troops. Behe knows this, there is nothing like a little truth to get the evolution deniers spitting mad. That will rack up a few more sales for Behe. All this hubbub is in the details of the real science, Behe’s groupies don’t want to know the science. Behe has a good racket going, he lost (gave up) all credibility as a scientist (just look at all the Lehigh professors calling him a dolt because they are so embarrassed by his crackpottery), so now he must get his hugs from the creationist groupies – oh and a few buck for retirement won’t hurt either.

oh and a few buck for retirement won’t hurt either.

I hadn’t thought of that. Heck, if he’d retire sooner, I’ll buy a copy. There’s a lab at Lehigh gathering dust and plenty of young PhDs and post-docs ready and willing to step in and do some actual, y’know, research.


You may be on to something. Maybe we can just buy Behe out of creationism. I am afraid if he only retired, he would write even more junk.

One the one hand, I do feel for the poor soul. He has sold his soul. The stack of papers and books piled high in court was soooo embarrassing he was a mere whimpering heap. You could see him facing the reality of leaving his professionalism behind forever and demanding - ala a 2 year old - no it is not enough, nothing will ever be enough…

Here’s a howler. Part three of the Behe reply to Musgrave (because ERV was so mean to me) is up. And he STILL can’t face the reality of the viroporin role for Vpu

To answer Dr. Musgrave’s question, I wouldn’t list this as a new binding site, not because it doesn’t bind a cellular protein, but because, as I explicitly state in the book, I place viral protein-cellular protein interactions in a separate category. My book concerns cellular protein-protein binding sites (or new viral-viral sites).

Ahem, Dr. Biochemist. The pentameric viroporin is due to new viral-viral sites.

Well, it is abundantly obvious that Behe has forgotten more biochemistry than he ever knew. Quite a skill, pity it’s so absurd.

no hugs for thugs, Shirley Knott

I am not certain since this not my area of expertise. How could it possibly matter what “class” he wants to call a new binding site. A new, functional, and advantageous binding site is, well a new, functional and advantageous binding site.

I guess all advantageous evolutionary changes could be classified in a group that creationists are not talking about - thus there are no advantageous evolutionary changes … ummm.

Someone really needs to unpack Behe’s brain, but this approach is patently ridiculous.

This argument is abotu proteins binding in viruses. Despite all the fance techno babel the fact remeains that viruses are decayed living things. Behe’s arguments pertain to new introductions of living organisms not their dead carcases floating through space time. Yes small scale evolution happens. Behe believes even in large scale evo. But you cant put 40 parts on top of a subsystem via the darwinian pathway. There is no benefit to small accumulations of parts that dont function until you get 40 of them together working as a single unit. How do all of these parts just come together improbabilistically? That is why Behe is a Design Theroist. He looks at irreducibly complex biology from the perspective of a designer. In other words he asks himself “how could i design this?” And “what resources would it take to purchase this kind of system.” No one knows if their is an intelligent designer as in the form of a being out there somewhere. Behe just detects or infers design when he sees IC. This is a very fertile and interesting perspective for science especially since we have had so much trouble dealing with degenerative illnesses. Maybe we can reverse engineer them in a sense because the status quoe is really quite sad.

About this Entry

This page contains a single entry by Ian Musgrave published on November 13, 2007 5:53 PM.

November 13 2007: Countdown to “Judgment Day: Intelligent Design on Trial” was the previous entry in this blog.

Liveblogging Judgment Day is the next entry in this blog.

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