Michael Behe

The Journal of Eukaryotic Microbiology recently published several papers from a workshop sponsored by the International Society of Protistologists titled “Horizontal Gene Transfer and Phylogenetic Evolution Debunk Intelligent Design.” So here we have a respected scientific society, presumably planning a workshop months in advance, and finally laying out their considered case for why intelligent design fails. As you might imagine, I was most anxious to read about it. Unfortunately, rather than scholarly papers, the manuscripts read like press releases from the National Center for (Darwinian) Science Education. So the introductory essay¹ by Avelina Espinosa tells us that ID has “creationist beginnings,” claims that I say “evolution” is “impossible,” and places in my mouth the phrase “design creationism” (I have never uttered that phrase except to disparage it). Blah, blah, blah. About as much scholarship as you’d get from a typical politician.

I recently received an email asking if the correspondent correctly understood my views about intelligent design and God. Since I sometimes get similar questions, I’m posting this correspondence for anyone who is interested.

Q: I understand your current position to be that design is detectable in nature, and that design detection is not merely a theological gloss upon the scientific facts, but is actually an activity appropriate for science. I further understand you to be saying that design detection in itself is neutral regarding the way that the design found its way into nature. Thus, if the bacterial flagellum is designed, it *could* be that God took a regular bacterium and miraculously “tweaked” it, or it *could* be that God “front-loaded” the evolutionary development of the bacterial flagellum, in a manner similar to that suggested by, say, Michael Denton. Design detection as a science cannot rule on these things; all that it can show is that Darwinian mechanisms, all by themselves, could not have produced integrated structures such as the flagellum. If there was not direct intervention (tweaking, guiding, steering, etc.) or advance planning (“front-loading”), neo-Darwinian processes would never have been able to produce all the complex varieties of living things that we see today. Have I got your current position correct?

Me: Yes, that’s exactly right.

Q: Then there is the question whether your views have changed over the years. Someone I know claims that in your early writings and early conference appearances, you said directly, or gave the strong impression, that some things (A, B, C …) were brought about by wholly natural processes, whereas other things (X, Y, Z …) were brought about by design (the implication being that “designed” in your early thought was opposed to “natural”). My acquaintance’s picture of Behean evolution would then be something like this: evolution in the early oceans chugs along on its own, via neo-Darwinian and other stochastic processes, as various sorts of marine worms and sponges and so on develop. But then, during the Cambrian Explosion, God takes a direct hand and literally reshapes marine worms into 30 or so new phyla, after which things go on by natural means again, until the next limit is reached, and God has to disrupt the normal flow of nature again (maybe to create land animals, or mammals, or birds, or man). Thus, there would be a jerky, stop-and-start sort of evolution, with chance/natural law causes alternating with fits of miracles. So, looking at any given creature, science would have to say things like: “Human lungs — evolved by blind mechanisms from primitive air bladder; human camera eye — required special intervention from intelligent designer; bacterial cell walls — evolved by blind chemical mechanisms; bacterial flagellum — was made by a bolt of divine lightning.” Etc. Given this understanding of your views, one can see why my acquaintance or other TEs would characterize ID as “God of the gaps” reasoning. My question is: Was it *ever* your view that ID *required* such a jerky view of evolution, and more generally that it required miraculous intervention (breaking the causal nexus, violating the laws of nature)? Or was it always the case that your view *allowed for* jerky, stop-and-start evolution, and *allowed for* miraculous intervention, but did not *require* these things?

The science writer Carl Zimmer posted an invited reply on his blog from Joseph Thornton of the University of Oregon to my recent comments about Thornton’s work. This is the last of four posts addressing it. References appear at the bottom of this post.

At the end of his post Thornton waxes wroth.

Behe’s argument has no scientific merit. It is based on a misunderstanding of the fundamental processes of molecular evolution and a failure to appreciate the nature of probability itself. There is no scientific controversy about whether natural processes can drive the evolution of complex proteins. The work of my research group should not be misintepreted by those who would like to pretend that there is.

Well, now. I’ll leave it to the reader of my previous replies to Thornton to decide whether she thinks they have scientific merit, and whether it is I or he who misunderstands the disputed facets of molecular evolution. As for “the nature of probability itself” and “no scientific controversy,” I will briefly address those here.

The science writer Carl Zimmer posted an invited reply on his blog from Joseph Thornton of the University of Oregon to my recent comments about Thornton’s work. This is the third of several posts addressing it. References will appear in the last post.

Now back to Thornton’s first point, the role of neutral mutations (which he sometimes labels “permissive” mutations). At several places in his post Thornton implies I’m unaware of the possibilities opened up by genetic drift:

Behe’s discussion of our 2009 paper in Nature is a gross misreading because it ignores the importance of neutral pathways in protein evolution…. Behe’s first error is to ignore the fact that adaptive combinations of mutations can and do evolve by pathways involving neutral intermediates…. As Fig. 4 in our paper shows, there are several pathways back to the ancestral sequence that pass only through steps that are neutral or beneficial with respect to the protein’s functions.

My interest in evolution by neutral mutation, however, is a matter of public record. It is an old idea that if a gene for a protein duplicates (3), then multiple mutations can accumulate in a neutral fashion in the “spare” gene copy, even if those mutations would be severely deleterious if they occurred in a single-copy gene. Four years ago David Snoke and I wrote a paper entitled “Simulating evolution by gene duplication of protein features that require multiple amino acid residues” (4) where we investigated aspects of that scenario. The bottom line is that, although by assumption of the model anything is possible, when evolution must pass through multiple neutral steps the wind goes out of Darwinian sails, and a drifting voyage can take a very, very long time indeed. But don’t just take my word for it — listen to Professor Thornton (1):

The science writer Carl Zimmer posted an invited reply on his blog from Joseph Thornton of the University of Oregon to my recent comments about Thornton’s work. This is the second of several posts addressing it. References will appear in the last post.

Now to Professor Thornton’s reply. He writes at length but makes just two substantive points: 1) that neutral mutations occur and can serendipitously help a protein evolve some function (“[Behe] ignores the key role of genetic drift in evolution”); and 2) that just because a protein may not be able to evolve a particular function one way does not mean that it, or some other kind of protein, can’t evolve the function another way (“nothing in our results implies that, if selection were to favor the ancestral function again, the protein could not adapt by evolving a different, convergent, underlying basis for the function”).

I’ll start with the second point since I can just quote myself to answer it. I wrote in one of my previous posts on Thornton’s work:

The science writer Carl Zimmer posted an invited reply on his blog from Joseph Thornton of the University of Oregon to my recent comments about Thornton’s work. This is the first of several posts addressing it. References will appear in the last post.

I must say, it never ceases to amaze me how otherwise-very-smart folks like Zimmer and Thornton fail to grasp pretty simple points when it comes to problems for Darwinian mechanisms. Let me start slowly with a petty complaint in Carl Zimmer’s intro to the post. Zimmer is annoyed that I think Thornton’s latest work is “great,” yet I thought his previous work published a few years ago was “piddling.” “Why the change of heart?” wonders Zimmer.

A new paper from Richard Lenski’s group has appeared in Nature and has garnered a fair amount of press attention. Some people asked me for my thoughts about it.

The new paper continues the grand experiment that Lenski has been publishing about lo these many years — allowing a culture of the bacterium E. coli to continuously grow and evolve under his close observation. The only really new thing reported is a technical improvement — these days one can have the entire genome of E. coli “re-sequenced” (that is, determine the sequence of the entire DNA of the particular E. coli you’re working with) done for an affordable cost. (There are companies which will do it for a fee.) So Lenski and collaborators had the whole genomes — each and every nucleotide — sequenced of the E. coli that they have been growing for the past twenty years. Since they froze away portions of their bacterial culture at different times along the way, they now have the exact sequences of the evolving culture at many time points, from inception to 2000 generations to 10,000 to 40,000. Thus they can know exactly which mutations appeared when — an almost-complete paper trail. Very very cool!

Nature has recently published an interesting paper which places severe limits on Darwinian evolution. The manuscript, from the laboratory of Joseph Thornton at the University of Oregon, is titled “An epistatic ratchet constrains the direction of glucocorticoid receptor evolution”. The work is interpreted by its authors within a standard Darwinian framework, but the results line up very well with arguments I made in The Edge of Evolution. This is the last of three posts discussing it. (see here and here)

Bridgham et al (2009) are interested in the reversibility of evolution, and discuss their results in terms of something called “Dollo’s law.” Louis Dollo, an early 20th century paleobiologist, was interested in discerning phylogenies. He maintained that one could always distinguish ancestral forms from descendant forms. Stephen Jay Gould (1970) commented that Dollo’s “law” was not an empirical observation, but rather a postulate which he felt was necessary to properly construct phylogenies. Over the years the meaning of “Dollo’s law” transmogrified. In modern usage, the phrase has come to mean that complex traits, once lost, do not re-evolve in the same lineage. For example, whales do not re-evolve gills, even though they are aquatic creatures who descended from fish, because gills are a lost, complex trait in that lineage.

Nature has recently published an interesting paper which places severe limits on Darwinian evolution. The manuscript, from the laboratory of Joseph Thornton at the University of Oregon, is titled, “An epistatic ratchet constrains the direction of glucocorticoid receptor evolution.” The work is interpreted by its authors within a standard Darwinian framework, but the results line up very well with arguments I made in The Edge of Evolution. This is the second of several posts discussing it.

Using clever synthetic and analytical techniques, Bridgham et al (2009) show that the more recent hormone receptor protein that they synthesized, a GR-like protein, can’t easily revert to the ancestral structure and activity of an MR-like protein because its structure has been adjusted by selection to its present evolutionary task, and multiple amino acid changes would be needed to switch it back. That is a very general, extremely important point that deserves much more emphasis. In all cases — not just this one — natural selection is expected to hone a protein to suit its current activity, not to suit some future, alternate function. And that is a very strong reason why we should not expect a protein performing one function in a cell to easily be able to evolve another, different function by Darwinian means. In fact, the great work of Bridgham et al (2009) shows that it may not be do-able for Darwinian processes even to produce a protein performing a function very similar to that of a homologous protein.

Before reading their paper, even I would have happily conceded for the sake of argument that random mutation plus selection could convert an MR-like protein to a GR-like protein and back again, as many times as necessary. Now, thanks to the work of Bridgham et al (2009), even such apparently minor switches in structure and function are shown to be quite problematic. It seems Darwinian processes can’t manage to do even as much as I had thought.

Nature has published an interesting paper recently which places severe limits on Darwinian evolution. This is the first of several posts discussing it.

The manuscript, from the laboratory of Joseph Thornton at the University of Oregon, is titled “An epistatic ratchet constrains the direction of glucocorticoid receptor evolution.” The work is interpreted by its authors within a standard Darwinian framework. Nonetheless, like the important work over the years of Michigan State’s Richard Lenski on laboratory evolution of E. coli, which has shown trillions of bacteria evolving under selection for tens of thousands of generations yielding just broken genes and minor changes, the new work demonstrates the looming brick wall which confronts unguided evolution in at least one system. And it points strongly to the conclusion that such walls are common throughout all of biology.

In the paper Bridgham et al (2009) continue their earlier work on steroid hormone receptor evolution. Previously they had constructed in the laboratory a protein which they inferred to be the ancestral sequence of two modern hormone receptors abbreviated GR and MR (Bridgham et al 2006). They then showed that if they changed two amino acid residues in the inferred ancestral receptor protein into ones which occur in GR, they could change its binding specificity somewhat in the direction of modern GR’s specificity. (All the work was done on molecules in the laboratory. No measurements were made of the selective value of the changes in real organisms in nature. Thus any relevance to actual biology is speculative.) They surmised that a gene duplication plus sequence diversification could have given rise to MR and GR. As I wrote in a comment at the time, that was interesting work, and the conclusion was reasonable, but the result was exceedingly modest and well within the boundaries that an intelligent design proponent like myself would ascribe to Darwinian processes. After all, the starting point was a protein which binds several steroid hormones, and the ending point was a slightly different protein that binds the same steroid hormones with slightly different strengths. How hard could that be?