Methinks it is sort-of like two weasels

[lee_merrill]

@Mercer

@lee_merrill

Taking into account existing variation, here.

Mentioning it, but not including it in any of his simplistic calculations.

But again, evolution had a chance to use existing variation in evolving chloroquine resistance, Behe thus did not exclude it in his 1 in 10^20 number,

@lee_merrill

… lots of spurious protein-protein interactions are already present inside the cell.

Well, that’s fine, but Behe is interested in new interactions, as in ones not based on already-existing mutations.

Meaning already-existing protein-protein interactions, sorry that wasn’t clear.

@Mercer

@lee_merrill

That’s what Summers et al. found out.

No, you are misrepresenting the paper. Did they assay all the mutants known in 2014? Have other mutants been identified since then?

“We measured the ability of more than 100 variants of PfCRT to transport CQ…” So they got a good sample, even though it may not be exhaustive.

@Mercer

@lee_merrill

And without pressure from chloroquine, the variants with resistance disappear,

Isn’t that precisely what happens in the phases of the Plasmodium life cycle in mosquitoes and rats? Is the fitness of these mutants higher or lower than wild-type in the absence of chloroquine, Lee?

Please show me where anything resembling that is included in Behe’s calculation.

The fitness of the mutants is lower than wild-type in the absence of chloroquine, would be the claim. So then treating the two mutations in each known path as deleterious singly, would explain why Behe states that both mutations need to occur together, to get the beneficial result.

@Mercer

Why do Summers et al. refer to haplotypes, but Behe never uses the word in the book?

I don’t know why this is important–but Behe references a paper that mentions haplotypes, in reference to sickle-cell mutations.

@Mercer

Why does Behe never mention epistasis?

Because evolution had this at its disposal, during the time chloroquine was in widespread use.

@Mercer

@lee_merrill

Behe doesn’t make a direct correspondence with protein-protein binding and PfCRT evolution, though. Have you read his argument?

I was responding to your claim that he does, remember?

@lee_merrill

Yes, so Behe generalizes from chloroquine resistance to new protein-protein binding sites,

But I meant Behe’s argument, using the arrival of chloroquine resistance as what he calls a CCC (chloroquine-complexity cluster), and comparing that probability to the probability of getting a new protein-protein binding site.

@Mercer

No new gizmos or basic machinery. There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins. [21]

Reference 21 is
Wang, J
Trends Biochem Sci
Volume 27, Issue 3, 1 March 2002, Pages 122-126
Protein recognition by cell surface receptors: physiological receptors versus virus interactions

It has nothing to do with Behe’s claim.

I would assume HIV is not referenced in this paper about viruses and protein-protein interactions. That would then merit mention as a reference.