This is the fourth in a series of posts responding to the extended critique of Darwin Devolves by Richard Lenski at his blog, Telliamed Revisited. Professor Lenski is perhaps the most qualified scientist in the world to analyze the arguments of my book. He is the Hannah Distinguished Professor of Microbial Ecology at Michigan State University, a MacArthur (“Genius Award”) Fellow, and a member of the National Academy of Sciences with hundreds of publications. He also has a strong interest in the history and philosophy of science. His own laboratory evolution work is a central focus of the book. I am very grateful to Professor Lenski for taking time to assess Darwin Devolves. His comments will allow interested readers to quickly gauge the relative strength of arguments against the book’s thesis.
“Solid and Interesting”
In his fourth post, “Evolution goes viral! (And how real science works),” Professor Lenski revisits a series of experiments on the bacteriophage lambda begun by his lab around 2012. Briefly, bacteriophages are viruses that invade and eat bacterial cells. Lambda specializes in eating E. coli cells. In order to invade the cell, lambda has to bind to a specific bacterial membrane protein, dubbed LamB, to gain a foothold. The Michigan lab grew a strain of E. coli that had lost much (but not all) of its ability to make LamB, together in a culture with bacteriophage lambda. The lambda had a much more difficult time invading those bacterial cells than normal ones, since its docking site was much rarer.
Over time, however, lambda acquired mutations in the protein (called “J”) that is responsible for binding LamB of E. coli. The mutations allowed it to bind to a second E. coli membrane protein, OmpF. Mutant phages could then invade cells that were unavailable to unmutated phages, so they prospered. When Lenski’s then-student Justin Meyer investigated, he saw that at least four specific amino acid changes had occurred, and all of them were necessary for the new ability to bind OmpF. Lenski’s current post emphasizes that requirement for multiple mutations, so the new interaction seems to him to be irreducibly complex and beyond the “edge of evolution.” What’s more, nothing was broken, so that contradicts the main argument of Darwin Devolves, he thinks.
I disagree. As I commented on the paper soon after it was published, “As always, the work of the Lenski lab is solid and interesting, but is spun like a top to make it appear to support Darwinian evolution more than it does.” Other instances of viruses adapting to new hosts with surface proteins that are structurally similar (as are LamB and OmpF) to the old binding site had been known for a while. What’s more, as Lenski’s lab later showed, the mutational pathway simply increased the initial strength of binding to the original protein until it also bound the structurally similar one. As I pointed out in The Edge of Evolution and emphasized in my reply to Sean Carroll’s unfavorable review of the book in Science, the fact that some properties can develop gradually does not mean that all can (such as the book’s major example of chloroquine resistance). Thus the new lambda function is neither irreducibly complex nor beyond the edge of evolution.
As far as nothing being broken, that, too, is incorrect. As I wrote at the time, in fact two E. coli genes were broken in order to escape infection, first by the original lambda and then by the mutated one.
But Not “Gain-of-FCT”
Professor Lenski seems to be annoyed with me over terminology.
Behe called lambda’s new ability to infect via the OmpF receptor a modification of function, instead of a gain of function, based on his peculiar definition, whereby a gain of function is claimed to occur only if an entirely new gene “poofs” into existence.
(I addressed Lenski’s incorrect “poofs” assertion in my last post.) I admit to using inexact wording in the 2012 comment. However, as a rule I try to avoid the phrases “gain of function” and “loss of function” altogether because they are imprecise. As I wrote in The Quarterly Review of Biology in 2010, I focus on what I term gain- or loss-of-FCT. FCT (pronounced “fact”) is a (sort of) acronym for Functional Coded elemenT. As I wrote in my previous post in this series, a FCT can be any coded feature of a gene or protein such as: promoters; enhancers; insulators; Shine-Dalgarno sequences; protein coding sequences; protein binding sites, organellar targeting- or localization signals; intron/extron splice sites, etc. (Some of those could potentially be formed by the switch of a single nucleotide — no “poofing” required.) It is coded elements such as those that underlie life, and a critical evaluation of Darwin’s mechanism to produce them has been sorely neglected in experimental evolution studies.
As I wrote in 2012, in my classification scheme I would categorize the ability of mutated lambda to bind to OmpF as a “modification of function” precisely because it is using the very same site on the J protein that it uses to bind to LamB. If it used a different area of the protein — one that had not previously been involved in protein binding (such as is the case with the sickle hemoglobin mutation, which I label a gain-of-FCT) — or a protein other than J, then I would call it a “gain-of-FCT.” I am not using “sleight of hand.” as Professor Lenski complains. Rather, I am trying to make critical and overlooked distinctions.
What the Data Show
For some reason, that seems not to be welcomed. Lenski writes in bold type, “To make his strange argument, Behe works very, very hard to convince readers that standard evolutionary processes are (i) really, really good at degrading functions, and (ii) really, really bad at producing anything new.” Well, yes, I do. And I do so because that’s what the data show — including the data of Lenski’s own (terrific) LTEE.
In Darwin Devolves I quote James Shapiro’s observation that “as many biologists have argued since the 19th Century, random changes would overwhelmingly tend to degrade intricately organized systems rather than adapt them to new functions.” If the results of modern science show those biologists to have been correct, why the reluctance to let people know?