After reviewing the effects of mutations upon Functional Coding ElemenTs (FCTs), Michael Behe’s recent review article in Quarterly Review of Biology, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” offers some conclusions. In particular, as the title suggests, Behe introduces a rule of thumb he calls the “The First Rule of Adaptive Evolution”: “Break or blunt any functional coded element whose loss would yield a net fitness gain.” In essence, what Behe means is that mutations that cause loss-of-FCT are going to be far more likely and thus far more common than those which gain a functional coding element. In fact, he writes: “the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.” Since organisms will tend to evolve along the most likely pathway, they will tend to break or lose an FCT before gaining a new one. He explains:
It is called the “first” rule because the rate of mutations that diminish the function of a feature is expected to be much higher than the rate of appearance of a new feature, so adaptive loss-of-FCT or modification-of-function mutations that decrease activity are expected to appear first, by far, in a population under selective pressure.
(Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
Behe argues that this point is empirically supported by the research reviews in the paper. He writes:
As seen in Tables 2 through 4, the large majority of experimental adaptive mutations are loss-of-FCT or modification-of-function mutations. In fact, leaving out those experiments with viruses in which specific genetic elements were intentionally deleted and then restored by subsequent evolution, only two gain-of-FCT events have been reported
After asking “Why is this the case?” Behe states, “One important factor is undoubtedly that the rate of appearance of loss-of-FCT mutations is much greater than the rate of construction of new functional coded elements.” He draws sound and defensible conclusions from the observed data:
Leaving aside gain-of-FCT for the moment, the work reviewed here shows that organisms do indeed adapt quickly in the laboratory–by loss-of-FCT and modification-of-function mutations. If such adaptive mutations also arrive first in the wild, as they of course would be expected to, then those will also be the kinds of mutations that are first available to selection in nature. … In general, if a sequence of genomic DNA is initially only one nucleotide removed from coding for an adaptive functional element, then a single simple point mutation could yield a gain-of-FCT. As seen in Table 5, several laboratory studies have achieved thousand to million-fold saturations of their test organisms with point mutations, and most of the studies reviewed here have at least single-fold saturation.
Thus, one would expect to have observed simple gain-of-FCT adaptive mutations that had sufficient selective value to outcompete more numerous loss-of- FCT or modification-of-function mutations in most experimental evolutionary studies, if they had indeed been available.
But this stark lack of examples of gain-of-functional coding elements can have important implications:
A tentative conclusion suggested by these results is that the complex genetic systems that are cells will often be able to adapt to selective pressure by effectively removing or diminishing one or more of their many functional coded elements.
Behe doesn’t claim that gain-of-function mutations will never occur, but the clear implication is that neo-Darwinists cannot forever rely on examples of loss or modification-of-FCT mutations to explain molecular evolution. At some point, there must be gain of function.
But if loss-of-function mutations are so much more common than gain-of-function mutations then the odds of a pathway following a multiple mutation pathway toward the construction of a new FCT before encountering a local adaptive peak that “breaks or blunts” the FCT may be prohibitively small. A short analogy will explain why:
Consider a hypothetical order of insects — let’s call them it Molecularevolutionoptera. Now let’s say that scientists discover there are 1 million known species of Molecularevolutionoptera, and that the extinction rate of Molecularevolutionoptera is 1000 species per millennium. But scientists also determine that the speciation rate is only 1 species per millennium. In such a case, there will be a net loss of 999 species per 1000 years. At these rates, mathematically speaking, by 1,000,001 years from now, there should be no species of Molecularevolutionoptera left alive on earth.
If Behe’s article is correct, then molecular evolution, in the world of real biology, faces a similar problem. Remember that Behe found that “the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.” If loss/modification-of-FCT adaptations are 100-1000 times more likely than gain-of-FCT adaptations, then logic dictates that eventually an evolving type of organism will run out of FCTs to lose/modify.
In short, the logical outcome of Behe’s finding is that some process other than natural selection and random mutation must be generating new FCTs. If Darwinian evolution is at work, it tends to remove FCTs much faster than it creates them — something else must be generating the information for new FCTs.
The evidence cited by Behe does not paint a hopeful state of affairs for Darwinian proponents of molecular evolution.