Way back when, @Ashwin_s asked:
Maybe some others can chime in here, but the following excerpt from Behe’s latest response to Lenski seems to be saying (or predicting) that all genes under positive selection will inevitably be “broken”. That seems to me to be both preposterous and testable.
The excerpt:
As I initially discussed in a book chapter and as I emphasize in Darwin Devolves , beneficial degradative mutations have a very strong, natural, built-in advantage over beneficial constructive ones, exactly because of their frequency of occurrence . Let me explain briefly here. Consider two genes, either of which when mutated would be beneficial for an organism to meet some particular selective challenge. The first gene (call it A ) would be helpful if it mutated (call the mutated protein A*) at a particular residue of the protein it coded for to give a new constructive feature (perhaps a helpful new binding site). The second gene (call it B ) would be helpful if it mutated (to B*) so that its activity were substantially degraded or eliminated entirely. Yet there are orders of magnitude — a hundred to a thousand — more ways to degrade B than to improve A . That means that if neither mutation were originally present in the population of a species, B* would be expected to appear in only a hundredth to a thousandth of the time needed for A* to show up. For example, if in this situation the time expected for a constructive mutation to arrive were a hundred thousand years, a degradative mutation would arrive in only one hundred to one thousand years. The result is that B would have 99,ooo to 99,900 years to spread through the population to fixation before A* even showed up.* If both A* and B* relieve the same selective pressure, then when A* eventually did show up there would be no more pressure to relieve, since B* had done so long before. Thus B* has a built in advantage simply because it is degradative — because its mutation rate is much higher.
If a population is large enough to be expected to already contain some copies of A* and B*, then, simply because of the many more ways to break B to produce B*, there would be expected to be a hundred to a thousand times the number of the broken gene in the population compared to A*. That means it would have a hundred to a thousand times the chance of fixing before A*. Looking at it from a different angle, the selection coefficient for B* could be a hundred to a thousand times less that for A* and still have an equal chance to fix in the population first — to fix a degraded gene.