Apparently Behe is in a race to the bottom of the barrel in his latest “response”.
In this response he attempts to address the crippling of the central point in his book “Edge of Evolution”. His claim is that for malaria to develop resistance to CQ it must have two simultaneous mutations occur. Behe then took the probability of two specific mutations occurring simultaneously and tried to use it as a false “limit” of evolution. This is flat out wrong as clearly stated by the published literature. The literature clearly states that CQ resistance occurred gradually and that only having one gene mutation sill offers some resistance(in other words only having the one mutation is still beneficial instead of detrimental). The odds of two mutations occurring at the same time is irrelevant to CQ resistance in malaria and Behe knows it. Yet he keeps going back to it as if it does. Behe states:
“I stress in Chapter 3 that in the case of malarial resistance to chloroquine, multiple necessary mutations did happen in the membrane protein PfCRT. I also of course emphasize that it took a huge population size, one that would not be available to larger organisms.”
He also quote mined Carroll in a vain attempt to support himself. He quoted Carroll saying:
“Behe’s chief error is minimizing the power of natural selection to act cumulatively... Behe states correctly [my emphasis] that in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites.”
Let me fill in what Behe cut out of that quote: “...as traits or molecules evolve stepwise from one state to another via intermediates.”
Well, that changes things a bit. Behe is ignoring the fact that CQ resistance most likely occurred in multiple stages and then he had the audacity to take Carroll's quote out of context to give it the impression that Carroll was agreeing with his fictitious probability. The simply fact is that, yes, two mutations occurring at the same time IS very rare, but that has no bearing on Behe’s claims regarding CQ resistance in malaria since it did NOT require two simultaneous mutations. In breathtaking fashion, after ignoring cumulative gene mutation in CQ resistance and then quote mining Carroll, Behe then admits that mutations CAN occur in sequence and accumulate, but then he tries to dismiss it by saying, “it is a non sequitur to leap to the conclusion that all biological features therefore can gradually accumulate”. He tries to justify this by confusing his readers about beneficial and detrimental mutations. For one thing, natural selection filters out the detrimental mutations. Another more important fact is that the published literature clearly states that one gene mutation involved in CQ resistance imparts some resistance, and that resistance is ENHANCED by adding the second. The published works on CQ resistance are clear on this topic, CQ resistance most likely occurred gradually and the individual gene mutations ARE clearly beneficial. To watch Behe going through such contortions to try and defend his falsehoods is almost painful to watch.
Behe next attempts to address Carroll's demolishing of his claims about protein binding sites. Essentially Behe tried arguing in his book that binding sites are just too complex for evolution to account for. Carroll points out that this claim of Behe’s rests solely on Behe’s unfounded requirements for protein interaction. Carroll even ran through some simple math in his review that shows just how wrong Behe is:
“Very simple calculations indicate how easily such motifs evolve at random. If one assumes an average length of 400 amino acids for proteins and equal abundance of all amino acids, any given two-amino acid motif is likely to occur at random in every protein in a cell. (There are 399 dipeptide motifs in a 400-amino acid protein and 20 mult 20 = 400 possible dipeptide motifs.) Any specific three-amino acid motif will occur once at random in every 20 proteins and any four-amino acid motif will occur once in every 400 proteins. That means that, without any new mutations or natural selection, many sequences that are identical or close matches to many interaction motifs already exist. New motifs can arise readily at random, and any weak interaction can easily evolve, via random mutation and natural selection, to become a strong interaction (9). Furthermore, any pair of interacting proteins can readily recruit a third protein, and so forth, to form larger complexes. Indeed, it has been demonstrated that new protein interactions (10) and protein networks (11) can evolve fairly rapidly and are thus well within the limits of evolution.”
Behe’s only response to this is to misrepresent the cited references then to accuse Carroll of “begging the question” just as he did Jerry Coyne in his earlier “response”. Behe does nothing to address the fact that his assertion in regards to protein binding sites is fundamentally WRONG.
I was still willing to give Behe the benefit of the doubt about the errors in his book. I was willing to entertain the idea that maybe he just got in over his head and didn't understand the subjects he was talking about. The naked dishonesty Behe has demonstrated in this “response” has cinched my opinion, the “errors” in Behe’s book were deliberate.
You can read Carroll's review here:
http://www.sciencemag.org/cgi/content/full/316/5830/1427References:
CQ resistance
http://linkinghub.elsevier.com/retrieve/pii/S009286740080447Xpaper that Behe misrepresented
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16172400
There's quite a bit more after that.
You’re welcome for the link- infact, it does ‘go on’ and the points brought up by the poster you quoted are refuted once again in hte very next post- so let’s keep going here (And by hte way- nothign that was posted claiming Behe ‘quote miend’ was relevent- what was left out did nothign to udermine what Behe was stating- but let’s do pretend that it did, shall we?
“David Marshall says:
Your claim to objectivity, Mr. / Mrs Allen, is hard to believe, reading some of your other postings. But all right, let’s take your arguments at face value. Here, it seems to me, you’re missing the ball. You may even be swinging for the wrong fence.
Behe is not primarily making an apriori argument in this book. He is arguing from the actual history of evolution among pathogens. The point about chloroquine resistence is that in fact it has not arisen that often. Resistence to atovaquone, by contrast, appears to arise very quickly; every third person, he says. (59) He ascribes the difference to the fact that the former requires two mutations, the latter, just one.
If you want to refute Behe on this point, what you need to prove is that (1) CQ resistance actually demands more than two mutations. (To show that potentially profitable mutations arise more frequently than Behe claims), or (2) CQ resistance actually appears far more often — exponentially more often — than Behe claims.
If you can do one of these two things, then it seems to me that you will have made his position in this book less comfortable. Until then, you’re just batting theory around. In fact, some of your arguments seem to actually make his point stronger.”