Professor Coyne's first objection is: 1. In virtually none of the experiments summarized by Behe was there the possibility of adapting the way that many bacteria and viruses actually adapt in nature: by the uptake of DNA from other microbes. Lenski's studies of E. coli, for instance, and Bull's work on phage evolution, deliberately preclude the front of other species that could function as vectors of DNA, and therefore of new FCTs.
Coyne is only wrong here, at least about phages (bacterial viruses). Viruses grow in other organisms - the cells they infect. Thus pretty much by definition they are in touch with other microbes for lots of their life cycle, and it is thinking that sometimes viruses acquire genes from their host cells. In fact, in one study by Bull's group I reviewed, in which the factor for bacteriophage T7 ligase was intentionally removed at the beginning of an experiment, the investigators reported they initially expected the missing gene to be replaced. At the outset, our expectation from employment in other viral systems was that the release of ligase activity would stay so injurious to T7 that recovery to high fitness would take the genome to acquire new sequences through recombination or gene duplication and to replace ligase function by difference of those sequences. Unexpectedly, however, "This desire was not realized, and compensatory evolution occurred through point mutations and a deletion." Thus it seems that Professor Coyne's expectations about what is needed for a gain-of-FCT event are not universally shared among scientists.
Coyne is of course correct that in experiments in which only one species of bacteria is present, the cells cannot acquire DNA from other species of bacteria. Yet those who conducted such experiments often had expectations for evolution much different from him. In the seventies and eighties many workers thought that gene duplication or recruitment plus divergence would allow bacteria to broaden the foodstuffs they could metabolize. Out of many such experiments, only one seemed to go by gain-of-FCT. Professor Coyne's dismissal of such experiments is pure hindsight.
Professor Coyne doesn't mention that in the survey I contend that results from nature are harmonized with conclusions drawn from lab experiments. I wrote: One objection might be that the above examples are artificial. They concern laboratory evolution. Nonetheless, results arguably similar to those that have been seen in laboratory evolution studies to see have likewise been seen in nature, such as the release of many genes by Yersinia pestis (after, of course, the acquirement of new genetic material in the kind of several plasmids), and the loss-of-FCT mutations that make broadcast in human populations in reply to selective pressure from malaria. A tentative conclusion suggested by these results is that the complex genetic systems that are cells will oft be capable to conform to selective pressure by effectively removing or diminishing one or more of their many functional coded elements. Coyne's second objection is the following: 2. In relatively short-term lab experiments there has simply not been enough time to maintain the collection of complex FCTs, which consume time to make or acquire from a rare horizontal transmission event. I addressed that very spot in my review: Furthermore, although complex gain-of-FCT mutations likely would come only on long time-scales unavailable to laboratory studies, simple gain-of-FCT mutations need not get nearly as long. As seen in Table 1, a gain-of-FCT mutation in sickle hemoglobin is triggered by a mere point mutation, which helps code for a new protein binding site. It has been estimated that new transcription-factor binding sites in higher eukaryotes can be formed relatively quickly by one point mutations in DNA sequences that are already near matches (Stone and Wray 2001). In general, if a succession of genomic DNA is initially only one nucleotide removed from coding for an adaptive functional element, then a one simple point mutation could give 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 almost of the studies reviewed here have at least single-fold saturation. Thus, one would look 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. Yes, complex gain-of-FCT events would not be expected to occur, but simple GOF's would. Yet they didn't show up.
Professor Coyne then return to put words in my mouth: What [Be]he's saying is this: "Yes, gain of FCTs could, and probably is, more crucial in nature than seen in these short-term experiments. But my conclusions are modified to these types of short-term lab studies." No, that is not what I was saying at all. I was saying that, no matter what causes gain-of-FCT events to sporadically arise in nature (and I of course think the more complex ones likely resulted from deliberate intelligent design), short-term Darwinian evolution will be dominated by loss-of-FCT, which is itself an important, basic fact almost the tempo of evolution.
Above I quoted Coyne talking about "complex FCTs, which consume time to make or take from a rare horizontal transmission event." Yet cells aren't going to sit around twiddling their thumbs until that rare event shows up. Any mutation which confers an advantage at any time will be selected, and the great bulk of those in the dead term will be LOF. Ironically, Coyne seems to undervalue the king of natural selection, which "is casual and hourly scrutinising, throughout the world, every variation, even the slightest." A process which scrutinizes life "casual and hourly," as Darwin wrote, isn't going to look around for some rare event.
Professor Coyne's third objection is: 3. Finally, Behe does not mention-and I suppose he should have-the blanket and really solid grounds for adaptation via gain-of-FCT mutations in eukaryotes. As I read in Table 1 of the review, we have wonderful evidence of what Darwinian evolution has done to a multicellular eukaryotic species -- Homo sapiens -- in reply to strong selective pressure from malaria over the past ten thousand years. A smattering of mutations have been selected. The mutations are classified as: one GOF (the sickle mutation); two modification of functions; and five LOFs. That's pretty much the balance of what one sees in bacteria and larger viruses, so there is no cause to believe that short-term evolution in eukaryotes has a considerably different spectrum of adaptive mutations than for prokaryotes.
Coyne wants to concentrate on long-term evolution: While [eukaryotes] may occasionally acquire genes or genetic elements by horizontal transfer, we know that they gain new genes by the mechanics of gene duplication and divergence: new genes arise by duplication of old ones, and so the functions of these once-identical genes diverge as they learn new mutations. . Think of all the genes that have arisen in eukaryotes in this way and gained novel function: classic examples include genes of the immune system, Hox gene families, olfactory genes, and the globin genes. Unfortunately, Professor Coyne isn't making a vital distinction here. While we may know (or at least have really good grounds that is conformable with the idea) that new genes have arisen by duplication and divergence of old ones in eukaryotes, we do not recognize that happens by a Darwinian mechanism of random variation and natural selection. And if some duplicate genes do arise and diversify by Darwinian processes, we do not acknowledge that explains all or even most of them. After all, while the long-term processes that Professor Coyne envisions are winning their sweet time to get together, the quick and dirty short-term adaptive processes will dominate. That's what we know from the great efforts put into experimental evolutionary studies by many investigators over decades.
And as I point out in the QRB paper, all of this can be neatly summarized by The First Rule of Adaptive Evolution: Break or blunt any functional coded element whose loss would afford a net fitness gain.
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