Why is it that Darwinian rhetorical strategies often remind me of a Monty Python sketch? In this case, the one about the philosophy department at the University of Wollamaloo, where every faculty member is called Bruce and the departmental rules include “Rule two: No member of the faculty is to maltreat the Abbos [aboriginal Australians] in any way a’all — if there’s anyone watching.”
So Michael Behe amusingly notes in his Amazon blog how public Darwinian responses to the main argument of his book The Edge of Evolution differ from responses in more technical forums. Or as Bruce might put it, Rule one: No member of the Darwin Lobby may admit that evolution poses seemingly unsolvable enigmas — if there’s anyone watching.
When The Edge of Evolution came out, reviewers such as Sean Carroll at the U. of Wisconsin and Jerry Coyne at the U. of Chicago were full of reassuring noises for their readers in Science and The New Republic respectively. Behe had shown the insuperable difficulties evolution faces in explaining how multiple mutations can add up to results even as basic as the most elementary protein features, notably binding sites.

Coyne intoned, “In fact, interactions between proteins, like any complex interaction, were certainly built up step by mutational step … This process could have begun with weak protein-protein associations that were beneficial to the organism. These were then strengthened gradually…”
Uh huh. As Behe summarizes, the “take-home message of the reviews for the public and for scientists in other fields was the same: Nothing to see here, folks. Move along. No problem here.”
But in less publicly exposed venues, the mask of longstanding confidence comes off. Behe points to a recent paper seeking to clear up precisely the problem that Carroll and Coyne insisted upon as being non-existent. Appearing in the online journal Biology Direct, the paper is accompanied by comments from journal editor Eugene Koonin. He congratulates the authors on their “brilliant,” “novel solution” to “the old enigma of the evolution of complex features in proteins that require two or more mutations [emphasis added].”
That would be the same old enigma that, when in the public eye, Darwin’s defenders are so zealous to deny as being enigmatic at all. Only when no one’s watching are the Bruces free to admit such things.
A different question is whether or not the enigma has indeed been solved. Behe thinks not. The Biology Direct authors claim that a source of mutations apart from that at the DNA level can give a sort of leg up, a “look ahead” effect, to the process of natural selection operating on random genetic mutations. When genes are translated into proteins, more mutations can occur than when DNA is replicating, so that, according to one estimate, 1 in 10 proteins is afflicted in this way.
Behe argues that this piece of speculation is itself afflicted in various ways, most importantly that it is merely speculative. Instead of focusing on such inherently inadequate models, it makes much more sense to take seriously the kind of actual data that properly constrains theoretical models.
Which happens to be the main point of The Edge of Evolution. Writes Behe:

To have a good idea of what Darwinian evolution can do, we no longer need to rely solely on speculative models, which may overlook or misjudge aspects of biology that nature would encounter. We already have good data in hand. We already have results that should constrain models. Over many thousands of generations, astronomical numbers of malarial cells seem not to have been able to take advantage of the look-ahead effect or anything else to build new, coherent molecular machinery. All that’s been seen in that system in response to antibiotics are a few point mutations. In tens of thousands of generations, with a cumulative population size in the trillions, no coherent new systems have been seen in the fascinating work of Richard Lenski on the laboratory evolution of E. coli. Instead, even beneficial mutations have turned out to be degradative ones, where previously functioning genes are deleted or made less effective. And that’s the same result as has been seen in the human genome in response to selective pressure due to malaria — a number of degraded genes or regulatory elements, and no new machinery.