Methinks it is sort-of like two weasels

[Mercer (John Mercer)]

@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,

He did exclude it, because Behe falsely claims that everything has to come from new mutations. That necessarily excludes existing variation.

@lee_merrill

@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.

Most new interactions begin as already-existing ones.

@lee_merrill

@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.

How good? How exhaustive? What are the numbers? You don’t have the slightest idea, but you’ll say anything to defend it. Why?

@lee_merrill

@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.

No, the fitness could be the same. You’re missing the point by a mile.

@lee_merrill

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.

Or, intermittent selection explains the low frequency of fixation.

@lee_merrill

@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.

So what? What does the term mean? What if two different mutations are on different alleles? Let’s see, might there a way to get them together in the same allele? You won’t learn this from Behe.

@lee_merrill

@Mercer

Why does Behe never mention epistasis?

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

But he never considers it as a mechanism. Why? Does he think that his readers aren’t very smart?

@lee_merrill

@Mercer

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.

Doing that is academic misconduct. Look at how reflexively you make up silly reasons–even when you already know that Behe’s claim of zero is objectively false!