Miller Reviews EoE

Ken Miller has now published his review of Behe's latest. He did an excellent job. I think he really nailed some of Behe's more egregious mathematical errors:

Behe, incredibly, thinks he has determined the odds of a mutation "of the same complexity" occurring in the human line. He hasn't. What he has actually done is to determine the odds of these two exact mutations occurring simultaneously at precisely the same position in exactly the same gene in a single individual. He then leads his unsuspecting readers to believe that this spurious calculation is a hard and fast statistical barrier to the accumulation of enough variation to drive darwinian evolution.

It would be difficult to imagine a more breathtaking abuse of statistical genetics.

Behe obtains his probabilities by considering each mutation as an independent event, ruling out any role for cumulative selection, and requiring evolution to achieve an exact, predetermined result. Not only are each of these conditions unrealistic, but they do not apply even in the case of his chosen example. First, he overlooks the existence of chloroquine-resistant strains of malaria lacking one of the mutations he claims to be essential (at position 220). This matters, because it shows that there are several mutational routes to effective drug resistance. Second, and more importantly, Behe waves away evidence suggesting that chloroquine resistance may be the result of sequential, not simultaneous, mutations (Science 298, 74-75; 2002), boosted by the so-called ARMD (accelerated resistance to multiple drugs) phenotype, which is itself drug induced.

Behe's casual use of probability was something that really struck me about the book. The probability of obtaining enough favorable mutations to drive significant evolutionary change depends on so many variables that no simple calculation could possibly encompass enough of them to be meaningful. Using specific examples such as malaria to derive sweeping general conclusions about what evolution can and can not do is rather dubious logic, to say the least. The fact is we have ample indirect evidence that complex systems are the result of the gradual accretion of random variations. If a particular mathematical model says that such a thing is not possible, it is almost certainly the mathematics that must yield.

More like this

Another review of Behe's book, The Edge of Evolution, has been published, this time in Nature and by Ken Miller. This one focuses on Behe's central claim, that he has identified a probabilistic limit to what evolution can do that means no differences above roughly the genus level (and in many cases…
He keeps saying the same ol' debunked crap over and over again, and nowadays when a paper comes out that shows he was completely wrong about something, he spins it into a triumphant vindication for his sycophantic fans, who are all, apparently, abysmally innumerate. The hobby horse he's been riding…
Once again, Casey Luskin demonstrates that he's a biological ignoramus. He is much buoyed by a science report that chloroquinone resistance in the malaria parasite requires two mutations, claims that Michael Behe has been vindicated because that's exactly what he said, and demands an apology from…
A while back, I responded to Behe/Luskin's claim that his model proving the impossibility of evolution of chloroquinone resistance was vindicated. I pointed out (as did Ken Miller) that showing that a particular trait required multiple point mutations did not affect the probability in the naive way…

Rats, I wish I had access to Nature.

:(

By John Farrell (not verified) on 27 Jun 2007 #permalink

Behe's huffing and puffing response on Amazon (that Chris Harrison points us to) is quite amusing!

Behe dismisses the reaming he got at Dover:
If [Jerry] Coyne himself can�t explain how Darwinism can cope with the challenges The Edge of Evolution cites, how could a non-scientist judge?

Let's turn that type of logic on its head, shall we? If a non-scientist judge can understand how natural selection works and how it explains evolution, how could a biologist like Behe not understand it?

Irreducibly complex? No, irredeemably crass.

By Sam the Centipede (not verified) on 27 Jun 2007 #permalink

Dr. Rosenhouse:

He did an excellent job.

I have access to the papers Miller referenced, and have read them, and more. I learned the importance of doings so from you.

I posted my thoughts here: Ken Miller, the honest Darwinist.

regards,
Salvador

PS
By the way, in reciprocity, if there is something you would like the UD readers to be aware of from your weblog, I'm happy to advertise it there on your behalf. I was very delighted to point them to your recent blog, Coyne Lays and Egg

By Salvador T. Cordova (not verified) on 28 Jun 2007 #permalink

I found Behe's attempts to respond to his critics amusing. With respect to Carroll's review, which points out that very small motifs can be sufficient for protein binding, Behe replies

Wow, every protein in the cell will have a binding site! Methinks Carroll has just stumbled over an embarrassment of riches. If every protein (or even a large fraction of proteins) had such a binding site, then binding would essentially be non specific.

Has Behe really never done a binding experiment? If he had, he would have been confronted with the ubiquity of nonspecific binding. Yes, just about everything does bind nonspecifically to everything. Of course, this kind of relatively low-affinity promiscuous binding is inefficient, but it could still have selective value if the complex thus formed results in a useful structural assembly or a valuable enzymatic activity. This sort of ubiquitous nonspecific binding provides a basis for evolutionary optimization, where successive mutation result in gradually increased affinity (and therefore increased specificity). His other argument is that not every protein with a "phosphorylation motif" is phosphorylated in vivo. Here he commits the classic blunder of examining a modern cell and assuming that its evolutionary precursor must have possessed all of the same features and capabilities. In fact, a phosphorylation motif is merely a necessary but not sufficient condition for phosphorylation in vivo. After all, there have been millions of years of evolution to hone specificity. Mechanisms of specificity include accessory proteins that effectively direct kinases to specific proteins, as well as other motifs that enhance the affinity (and hence specificity) of the basic phosphorylation motif.

These are fairly basic biological errors. Is Behe really serious, or is he willing to utilize even arguments that he knows to be fallacious?