@Mung A Hunt and N Lents recently addressed Behe’s book here:
“Accidental” carries different implications. It implies that proteins have intent. They don’t. Mutations are just what biology does. Mutations are no more an accident than a hurricane is an accident.
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Where does Behe support this claim?
In brewers yeast, the rate of gene loss and gene gain balance out so that the yeast keep about the same number of genes through time:
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Really, to see why Behe’s focus on the prevalence of “degenerative” adaptive mutations does not lead to the conclusion that evolution could not amount to enough of an increase in adaptive complexity to produce the kinds of molecular complexity we see in extant organisms, one has merely to read Arlin Stoltzfus’s original 1999 paper on The possibility of constructive neutral evolution. (Accessed freely here: https://philpapers.org/archive/STOOTP)
Many of the purported “loss of function” mutations identified by Behe fit perfectly well into molels of constructive neutral evolution.
The basic scenario is as something along the following lines: Already existing functional genes are duplicated. These duplicates frequently acquire their own promoters, either by being duplicated into a different area under control of an already existing promoter, or by a promoter region being duplicated into an area upstream of an existing ORF.
This is textbook exaptation, but under Behe’s definitions would NOT qualify as gain of function (which is very misleading as I will argue below), because both the gene and the promoter keep doing, at a biochemical level, what they were already doing. The promoter region still just recruits the same transcription factors and initiate expression of downstream genes, and the ORF still produces the same protein coding or RNA gene with, at least initially, the same biochemical function.
These entities can now diverge in function. The expression timing of the already existing gene that was copied, and the new copy having acquired it’s own promoter, can now diverge. Even if this is adaptive, Behe would not call it a “gain of function”, because they still do what they already did at a biochemical level. At best they would constitute “modifications of function” under Behe’s definitions.
This phenomenon can keep going through many iterations, as more and more genes are duplicated and can acquire adaptive novel expression patterns, many of them become redundant, or even deleterious, so their eventual loss can become beneficial. So we have adaptive “loss of function” of these excessive duplicate genes and promoters.
The overwhelming pattern is thus one of adaptive loss and modification of function, with a lot of neutral background divergence and duplication
Once in a rare while, one of these excessive duplicates can acquire an adaptive biochemical novel function that Behe would agree qualifies as a “gain of function”(he does, after all, agree this happens). But in their relative frequencies, the neutral duplications, the adaptive modifications, and the adaptive losses of function, would vastly outnumber what Behe would agree is a biochemical “gain of function” mutation.
But what is the overall picture here? What is the “net result” in terms of the magnitude of total molecular complexity of the cell? Or in terms of the total number of phenotypic functions? Well it is entirely possible we get an increase in molecular complexity and functions.
Because we get more and more genes, which become more and more diverged and specialized, of which many become pseudogenes. And once in a while, maybe one in a thousand, gain a new biochemical function. And many of the diverging duplicates, while they are biochemically just “modifications” or “losses” of functions, they can often times constitute adaptive gains of phenotypic functions(white polar bear fur). Another example could be antibiotic resistance. Novel regulation of a transporter gene, while biochemically a modification, or even a loss of function, could be a phenotypic gain of antibiotic resistance.
The total number of functions can actually easily increase. Because most of the functions being lost are diverged copies, paralogous genes having acquired their own regulation, this has the effect of looking like mostly “degenerative” adaptive evolution at the molecular/biochemical level.
Because Behe doesn’t define the novel association between the copy of an already existing protein coding gene, and an already existing promoter elsewhere in the genome, as a “gain of function” mutation, this has the effect of making it seem like the majority of molecular evolution is “degenerative”. What this means is Behe’s case is at bottom rhetorical, as it rests on how Behe defines what qualifies for a “gain of function”. And a novel association between already existing genetic elements, in so far as these distinct elements still biochemically perform the same function, will not qualify as “gain” by Behe.
The phenotypic effect of the association is explicitly ignored in favor of the biochemical effect. To pick an example, the cit+ mutation in the LTEE is a “modification of function” mutation under Behe’s definition, because at the biochemical level, the promoter region still does what it always does. Since the citrate transporter, which is normally not expressed when oxygen is present, was duplicated into another area of the chromosome downstream of a promoter that expresses a set of genes when oxygen is present, the citrate transporter is now expressed with oxygen present.
But to Behe, this duplication is not a gain of function. The promoter under which the citrate transporter was duplicated still recruits the same transcription factors to regulate the expression of all those downstream genes, and the transporter gene still does what it always does, which is to transport citrate into the cell. So to Behe, this adaptive novel functions is only a “modification of FCT”.
But it is a PHENOTYPIC gain of function. The cells can now metabolize citrate when oxygen is present. In sum total, Behe has a rhetorical argument, based on very restrictive definitions. By focusing only on biochemical effects, and only on adaptive mutations, he can call evolution “degenerative”. But his grand conclusion doesn’t follow. The molecular complexity, and the many complex phenotypic adaptations of life could easily evolve, many of which involve classic Darwinian selection, but Behe would call it degenerative. Problem is, his designer isn’t actually needed to do anything, as many of the mechanisms of evolution are simply ignored by his very restrictive “first rule of adaptive molecular evolution”. The whole thing is, at bottom, a sleight of hand.
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