Posted: Jan 01, 2015 12:09 am
by Rumraket
Shrunk wrote:
Rumraket wrote:
BooBoo wrote:In a talk in South Korea, Michael Behe has admitted doing a "victory dance" in his office based on new evidence that he claims supports his ID contentions:

1. Chloroquine resistance does indeed require exceptionally rare, simultaneous, mutations (the edge of evolution):

This is Behe's original and wrong claim. Simultaneity is not required, and probably not how CCC evolves.

TBH, I'm not sure that Behe ever claimed that the mutations had to be simultaneous. It's confusing, though, because some of his calculations rely on the presumption of simultaneity, as I've pointed out above. But that may be because Behe just didn't understand the (high school level) math that was involved in his calculations.

Well, I don't have Behe's Edge of Evolution book so I can't check. I guess we will have to dig it up somewhere to really verify what is original claim is. Though it seems Kenneth Miller did the research here:

Parasites and Drugs
Behe’s “Edge” argument rests on two basic points. The first is that a beneficial, selectable trait
like chloroquine resistance can arise only after multiple, simultaneous mutations emerge at
random. The target for those mutations is the gene for PfCRT, a membrane transport protein. In
chloroquine resistant strains, mutant versions of this protein are able to pump the drug out of the
cell’s digestive vacuole, enabling the parasite to survive.

As Behe puts it, the data argue “that a first, required mutation to PfCRT is strongly deleterious,
while the second may partially rescue the normal, required function of the protein, plus confer
low chloroquine transport activity.”6 Since that first “required” mutation is so deleterious, it
couldn’t possibly spread through the population while waiting for the second to appear. Natural
selection would weed out the deleterious mutation unless the second one popped up beside it in
the same organism. That, according to Behe, accounts for the very low frequency of chloroquine
resistance and validates his analysis.
Quite frankly, he must be secretly hoping that nobody actually looks at the details in the PNAS

Looks like he really did, initially start out asserting that simultaneity of two mutations was required, because one was supposedly (in his view) so strongly deleterious it could never linger around in the population and wait for the other compensatory one to offset it's effect.

So he was wrong. Case closed. :lol: