Dave Ussery Ruminates about <i>The Edge of Evolution</i> - Evolution News & Views

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Dave Ussery Ruminates about The Edge of Evolution

The first part of Professor Ussery's review of The Edge of Evolution on the website BioLogos is mainly an exercise in throat clearing, where he describes his "philosophical and personal perspective," notes that he and I agree on common descent, and correctly points out that my book concerns the mechanism of evolution. In the second installment Dave begins to show that he somehow just doesn't get the big points of the book. In writing of the sickle cell and other antimalarial mutations which degrade the genome, I had said that they were "hurtful." He misunderstands this, writing, "the example [Behe] gives us is not a 'good mutation.'" But the sickle cell and other antimalarial mutations most certainly are "good" mutations in a Darwinian sense because they are adaptive -- they help the organism survive. Think of it -- it was already known that most mutations that have an observable effect are deleterious. But now we know that even "good," adaptive mutations frequently damage or break genes. That is a fact that seems to be off most Darwinists' radar screens, although it is a profound challenge to their theory.

Dave then first employs what turns out to be a frequent tool of his: citations of papers in the literature (implying they support his position) without even an attempt to explain how they pertain to the mechanism of evolution or the edge to Darwinian evolution that I argue for in my book. He cites one paper, "Origins, evolution, and phenotypic impact of new genes," without saying how it is known the genes arose by Darwinian processes or citing where it was that I said gene duplication and diversification couldn't produce new genes. (I said no such thing -- the book concerns the limits to Darwinian evolution; it does not say Darwinian processes can't do anything, and I discuss the likely Darwinian origins of genes for antifreeze proteins in the chapter "What Darwinism can do.") He cites another paper "about recent evolution of beneficial mutations in humans" without saying what those mutations are, whether they are simple or complex, or whether they are constructive or (like antimalarial mutations) degradative. A reader of Dave's post would be quite surprised to discover that one of the last subsections of the article is called "Is Darwinian evolution enough?" where the author gingerly writes that non-Darwinian mechanisms (although -- God help us -- not intelligent design) "should not be categorically dismissed." Someone just might suspect that Dave is being misleading here, but I think it much more likely that he is so enchanted by Darwinian theory that he sees overwhelming evidence for it in any paper that contains the word "evolution."

Professor Ussery continues in this post with the oddest discussion of the role of mutation in Darwinian evolution that I have yet come across. He writes that I said it was astronomically improbable (an event of 1 in 10^20) that a protein should contain two mutations but, heck, he knows that some homologous proteins in different strains of E. coli have twenty mutations between them, so what's the problem? The problem is that for some specific effects (such as, say, chloroquine resistance) when a selective pressure arises one must switch two particular amino acid residues in a particular protein, not just any two in any protein. Take my word for it, that enormously affects the rarity of the event, most especially if one of the mutations by itself is detrimental. (If Dave thinks it is easy to build a multiresidue functional feature in a protein, then he should tell the prominent bioinformaticist Eugene Koonin, who recently worried about "the old enigma [my italics] of the evolution of complex features in proteins that require two or more mutations.") As an example of the power of mutation Dave writes that "One out of every 21 births in humans have some sort of STRUCTURAL change (and hence likely a functional change) in a protein, just from insertions from a single transposable element (alu), common in humans." Right. Inserting a transposable element into the gene for a working protein is like inserting a spear into someone's body. The structural change is overwhelmingly likely to destroy the protein's biological function. It's hard to have a productive dialog with a Darwinist who sees birth defects as evidence for the theory.

I discussed objections to my calculations of the improbability of multiple mutations at length years ago in response to printed reviews of The Edge of Evolution, and they are still online. Professor Ussery betrays no sign of having read them. He appears to think the discussion has begun fresh with his review.