In my last post I reported that University of Chicago evolutionary biologist Jerry Coyne, who had critiqued (http://tinyurl.com/2fjenlt) my recent Quarterly Review of Biology article (http://tinyurl.com/25c422s) concerning laboratory evolution studies of the last four decades and what they show us about evolution, had asked several other prominent scientists for comments (http://tinyurl.com/2cyetm7). I replied (http://tinyurl.com/4lq8sre) to those of experimental evolutionary biologist John Bull. In a subsequent post Coyne discussed (http://tinyurl.com/4tqoq7c) a recent paper (http://tinyurl.com/4shw456) by the group of fellow University of Chicago biologist Manyuan Long on gene duplication in fruitflies. After a bit of delay due to the holidays, I will comment on that here.
Try as one might to keep Darwinists focused on the data, some can’t help reverting to their favorite trope: questioning Darwinism simply must be based on religion. Unfortunately Professor Coyne succumbs to this. Introducing his blog post he writes:
What role does the appearance of new genes, versus simple changes in old ones, play in evolution? There are two reasons why this question has recently become important…. The first involves a scientific controversy…. The second controversy is religious. Some advocates of intelligent design (ID)—most notably Michael Behe in a recent paper—have implied not only that evolved new genes or new genetic “elements” (e.g., regulatory sequences) aren’t important in evolution, but that they play almost no role at all, especially compared to mutations that simply inactivate genes or make small changes, like single nucleotide substitutions, in existing genes. This is based on the religiously-motivated “theory” of ID, which maintains that new genetic information cannot arise by natural selection, but must installed [sic] in our genome by a magic poof from Jebus. [sic]
Anyone who reads the paper, however, knows my conclusions were based on the reviewed experiments of many labs over decades. Even Coyne knows this. In the very next sentence he writes, schizophrenically, “I’ve criticized Behe’s conclusions, which are based on laboratory studies of bacteria and viruses that virtually eliminated the possibility of seeing new genes arise, but I don’t want to reiterate my arguments here.” Yet if my conclusions are based on “laboratory studies”, then they ain’t “religious”, even if Coyne disagrees with them.
Professor Coyne is so upset, he imagines things that aren’t in the paper. (They are “implied”, you see.) So although I haven’t actually written it, supposedly I have “implied not only that evolved new genes or new genetic ‘elements’ … aren’t important in evolution, but that they play almost no role at all….” [Coyne’s emphasis]
“Play almost no role at all”? When I first read these “implied” words that Coyne wants to put in my mouth, I thought the argumentative move rang a bell. Sure enough, check out the Dilbert comic strip from November 1, 2001 (http://tinyurl.com/6y6upgc), where Dilbert complains that a co-worker “changed what I said into a bizarre absolute.” If one person says that an event is “very unlikely”, and an interlocutor rephrases that into “so, you say it’s logically impossible and would never happen even in an infinite multiverse”, well then, the second fellow is setting up a straw man.
Contrast Coyne’s imagined “implications” with what I actually wrote in the review. Considering possible objections to my conclusions I noted that:
A third objection could be that the time and population scales of even the most ambitious laboratory evolution experiments are dwarfed when compared to those of nature. It is certainly true that, over the long course of history, many critical gain-of-FCT events occurred. However, that does not lessen our understanding, based upon work by many laboratories over the course of decades, of how evolution works in the short term, or of how the incessant background of loss-of-FCT mutations may influence adaptation.
Although I think that statement is clear enough in the context of the paper, let me say it differently in case some folks are confused. Loss of function mutations occur relatively rapidly, and LOF mutations can be adaptive. Gain of function mutations can be adaptive, too, but their rate of occurrence (including the rate of gene duplication-plus-divergence that Coyne is discussing) is much less. Thus whenever a new selective pressure pops up, LOF adaptive mutations (if such there be in the particular circumstance) can appear most swiftly, and will likely dominate short-term adaptation. So when a GOF mutation eventually appears, it will likely be against the altered genetic background of the selective pressure ameliorated by the adaptive LOF mutation(s). In order to understand how evolution works in the long term, we must take that into consideration.
Professor Coyne notes that the new genes studied by Professor Long “arise quickly, at least on an evolutionary timescale”. [my emphasis] But adaptive LOF mutations arise quickly even on a laboratory timescale. For example, as I note in my QRB review, in one experiment (http://tinyurl.com/4zyxt66) adaptive mutations in E. coli cultures due to loss of function mutations in the rpoS gene “occurred, and indeed spread at rapid rates within a few generations of establishing glucose-limited chemostats”. A few generations for E. coli can be on the order of hours. The gene duplications studied by Professor Long occur on the order of millions of years. Admittedly the situation in nature is more complex than in the laboratory. Nonetheless, whatever selective pressures the gene duplications encounter when they eventually show up will already have been substantially altered by adaptive LOF mutations. That’s a very important point for evolutionary biologists to keep in mind.
I have never stated, nor do I think, that gene duplication and diversification cannot happen by Darwinian mechanisms, or that “they play almost no role at all” in the unfolding of life. (As a matter of fact, I discussed several examples of that in my 2007 book The Edge of Evolution. (http://tinyurl.com/4nqxhvr)) That would be silly — why would anyone with knowledge of basic biochemical mechanisms deny that, say, the two gamma-globin coding regions on human chromosome 11 resulted from the duplication of a single gamma-globin gene and then the alteration of a single codon? What I don’t think can happen is that duplication/ divergence by Darwinian mechanisms can build new, complex interactive molecular machines or pathways. Assuming (since he is in fact critiquing them) Professor Coyne has been attentive to my arguments, one background assumption that he may have left unexpressed is that he thinks the newer duplicated genes discovered by Professor Long’s excellent work represent such complex entities, or parts of them.
There is no reason to think so. A gene can duplicate and diversify without building a new machine or network, or even changing function much. The above example of the two gamma-globin genes shows that duplication does not necessarily result in change in function. The examples of delta- and epsilon-globin, which, like gamma-globin, presumably also resulted from the duplication of an ancestral beta-like globin gene, show that sequence can diversify further, but function remain very similar. Even myoglobin, which shares rather little sequence homology with the other globins, has not diverged much in biochemical function.
In his recent work Professor Long discovered that many of the new genes were essential for the viability of the organism — without the gene product, the fruitflies would die before maturity. Perhaps Professor Coyne thinks that that means the genes necessarily are parts of complex systems, or at least do something fundamentally new. Again, however, there is no reason to think so. The notion of “essential” genes is at best ambiguous. We know of examples of proteins that surely appear necessary, but whose genes are dispensable. The classic example is myoglobin (http://tinyurl.com/4ogmd98). It is also easy to conceive of a simple route to an “essential” duplicate gene that does little new. Suppose, for example, that some gene was duplicated. Although the duplication caused the organism to express more of the protein than was optimum, subsequent mutations in the promoter or protein sequence of one or both of the copies decreased the total activity of the protein to pre-duplication levels. Now, however, if one of the copies is deleted, there is not enough residual protein activity for the organism to survive. The new copy is now “essential”, although it does nothing that the original did not do.
To sum up, the important point of “Experimental Evolution, Loss-of-Function Mutations, and ‘The First Rule of Adaptive Evolution’” (http://tinyurl.com/25c422s) is not that anything in particular in evolution is absolutely ruled out. Rather, the point is that short term adaptation tends to be dominated by LOF mutations. And, tinkerer that it is, Darwinian evolution always works in the short term.
Here’s an analogy that some people might find amusing and helpful. Think of GOF mutations (such as the gene duplication/divergence that Professor Coyne discusses) as the “snail mail” of evolution. And think of LOF mutations as the email, texting, and phone calls of evolution. In a busy world, by the time a real letter shows up at someone’s or some business’s door, a lot of communication concerning the subject of the slow letter would already have happened by faster means, and the more important the topic, the more fast-communication there likely would have been. That speedy communication can quite easily change the context of the letter, and either render it moot or at least less important. It is certainly possible that on occasion the slow letter will arrive with its impact unaffected by other messages, but it would be foolish to ignore the effect of the fast channels of communication.