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 all of Behe’s critics.

Will Ken Miller, Jerry Coyne, Paul Gross, Nick Matzke, Sean Carroll, Richard Dawkins, and PZ Myers Now Apologize to Michael Behe?

No.

Here’s what his critics actually said. We have no problem with the idea that a particular functional phenotype requires a couple of mutations; I can think of lots of examples of that, such as the work of Joe Thornton on corticosteroid receptors. That the malaria parasite needs two mutations was never a point of contention, nor was it particularly worrisome. What was wrong with Behe’s work is that he naively claimed that the two mutations had to occur simultanously in the same individual organism, so that the probability that could happen was the product of multiplying the two individual probabilities. That’s ridiculous.

As Sean Carroll explained:

Behe’s main argument rests on the assertion that two or more simultaneous mutations are required for increases in biochemical complexity and that such changes are, except in rare circumstances, beyond the limit of evolution. .. Examples of cumulative selection changing multiple sites in evolving proteins include … pyrimethamine resistance in malarial parasites (6) — a notable omission given Behe’s extensive discussion of malarial drug resistance.

To show that the activity required two mutations, as the new paper says, is not an issue; it would have to claim that two simultaneous mutations were required, and that the cumulative accumulation of mutations in the population does not happen. And Behe goes further and declares on the basis of his bogus calculations that no evolution, beyond minor changes in a species or genus, occur at all.

So it’s weird to see Luskin announce that I’ve already conceded Behe’s point. No, I have not.

What we’ll probably get is nothing more than PZ Myers’s concession, offered in the context of the rant quoted above:

Fair enough; if you demand a very specific pair of amino acid changes in specific places in a specific protein, I agree, the odds are going to be very long on theoretical considerations alone, and the empirical evidence supports the claim of improbability for that specific combination.

Well, that’s more or less what’s required to generate chloroquine resistance. We’ll gladly take this — i.e., simply being proven right — in lieu of an apology.

Yet if you actually read the post in question, you’ll see that I’m not conceding that Behe is right — I’m explaining that a low probability is not a barrier to evolution.

Yet his argument for this dramatic conclusion is not only weak, it’s wrong. I could, for instance, correctly argue that the odds of getting a straight flush dealt to you in a 5 card poker hand is about 1 in 6×10⁴; we could calculate this with probability theory, and we could also deal lots of poker hands and determine it empirically. No one’s going to argue with that part of the math.

But now, if I were to define a Straight Flush Complexity Cluster (SFCC) parameter and wave it around and claim that “no hand of the same complexity as a straight flush has been dealt by chance in the last ten years of poker games here in town,” that players can only possibly win one hand in 60,000, or worse, that no one has won a poker hand without cheating and stacking the deck, you’d know I was crazy. But that is basically Behe’s entire argument — he claims to have found the “edge of evolution,” and that it is much sharper and steeper and more impassable than anyone but a creationist could believe.

I’m flattered that Luskin thinks a concession from me would be so significant, but he ought to wait until I’ve actually made one before declaring victory.

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Ken Miller wrote to second my comments:

With respect to the malaria mutations, your rebuttal is exactly correct. I’m attaching my review of Behe’s book in Nature. The portion of that review that directly deals with Behe’s contention about two mutations is this:

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.

Then, later on, I wrote:

“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.”

I hope these quotes are useful to you and your readers. As usual, Luskin is playing the “pretend” game of taking a new scientific paper and telling folks that it presents a “problem” for evolution. Ain’t life grand?

Best Wishes,

Ken