Pharyngula

Quote-mined by Casey Luskin!

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.

Comments

  1. […] By PZ Myers […]

  2. #2 Ashley Carter
    Long Beach, CA
    July 17, 2014

    Allow me to post a link to a paper I wrote as a grad student about fixations of double mutations I modeled the fixation time for pairs of novel mutations in which each is deleterious, but together they are advantageous. The main result is that drift can maintain the first mutation in a population long enough, even if deleterious, for the second to occur and then positive selection can fix the pair. The model described is for diploid populations, but the logic and process holds for haploid ones as well.

    People forget that variation in populations is how evolution often works in reality, it is not always via a stepwise process of monomorphic populations.

    http://rspb.royalsocietypublishing.org/content/269/1494/953.abstract

  3. #3 Raoul Duck
    Durham, NC
    July 17, 2014

    When you are dealing with 1:60000 odds in an insect species that hatches trillions of eggs each year, I’d dare say that the odds are pretty good.

  4. #4 Raoul Duck
    Durham, NC
    July 17, 2014

    Excuse the slip. Let me restate my point. When you are dealing with an amoeba that propagates zillions of times each year, 1:60000 odds are damn good.

  5. #5 Beau
    earth
    July 17, 2014

    Here’s a snippet from your 2007 review his book. You claim his rationale is poor in your review. Do you still stand by this?

    Several people have pointed out that his calculation of the frequency of evolution of cloroquine resistance seems dubious. Here’s his rationale.

    The mutant PfCRTs exhibit a rang of changes, affecting as few as four amino acids to as many as eight. However, the same two amino acid changes are almost always present—one switch at position number 76 and another at position 220.

    Since two particular amino acid changes occur in almost all of these cases, they both seem to be required for the primary activity by which the protein confers resistance.

    … [several pages later]

    …resistance to chloroquine has appeared fewer than ten times in the whole world in the past half century. Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance is roughly one in a hundred billion billion.

    That’s it. That’s the entire rationale. It’s very poor, and even granting it to him, it’s still not applicable to the whole problem of evolution.

  6. #6 Andrew
    July 18, 2014

    Have I misunderstood, or did Behe argue that a “CCC” is so improbable that it’s only happened several times in the past half century, therefore it couldn’t have happened by random mutation?

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