Uncommon Descent

2 November 2007

Trends in Ecology and Evolution follows the trend, Part I

Michael J Behe

Dear Readers,

The latest issue of the journal Trends in Ecology and Evolution (TREE) carries a tediously disdainful review (1) of The Edge of Evolution which revisits the blunders of previous reviews while adding new ones. This is the first of a three part series concerning the review. (References will be attached to the third part.)

Like almost all reviews by Darwinists, this one begins with a genuflection to the Dover trial, where a former-head-of-the-Pennsylvania-Liquor-Control-Boa rd-appointed-judge, showing no evidence he actually understood the academic arguments of either side, copied almost word for word the document handed to him at the end of the trial by the lawyers for the complainant. This was his “decision.” For signing off on a document castigating intelligent design the apparently clueless judge got his picture in Time magazine, was bequeathed honorary degrees, and has been lionized by all the right people. (On occasion I receive astonished inquiries from Europeans asking how Americans can allow a judge to rule on what are essentially philosophical matters. Good question — although it seems some European bureaucracies are getting in on the act now, too.) (2)

Scribes our TREE reviewer, “Behe begins by trying to shore up his argument that ‘irreducibly complex’ multiprotein systems, such as flagella, are unevolvable.” (1) Well, no, that’s not quite right. It seems he impatiently skipped a few chapters. My demonstration of the recently discovered greatly increased complexity of a number of biochemical systems is in the middle of the book. The argument of The Edge of Evolution actually begins in Chapter 2 by discussing the ravages that random mutation and natural selection have visited upon the human genome in its battle with the malarial parasite: sickle cell disease, thalassemia, G6PD deficiency and much more. I quote Carter and Mendis remarking:

This burden [of malaria] is composed not only of the direct effects of malaria but also of the great legacy of debilitating, and sometimes lethal, inherited diseases that have been selected under its impact in the past. (3, p. 589)

The importance of this discussion is that it sets the stage for the whole book by showing that random mutations much more easily debilitate genes than improve them, and that this is true even of the helpful mutations. Let me emphasize, our experience with malaria’s effects on humans (arguably our most highly studied genetic system) shows that most helpful mutations degrade genes. What’s more, as a group the mutations are incoherent, meaning that they are not adding up to some new system. They are just small changes — mostly degradative — in pre-existing, unrelated genes. The take-home lesson is that this is certainly not the kind of process we would expect to build the astonishingly elegant machinery of the cell. If random mutation plus selective pressure substantially trashes the human genome, why should we think that it would be a constructive force in the long term? There is no reason to think so.

No Darwinian reviewer of The Edge of Evolution has paused long to ponder the effects of malaria on the human genome. I wonder why.

26 October 2007

Kenneth R. Miller and the Problem of Evil, Part 3

Michael J Behe

(This is the third of three posts on Kenneth Miller and the problem of evil.)

I think the reason for Miller’s deep disdain of a relatively minor difference in our positions on evolution is not scientific. Rather, it’s theological. It’s called the problem of evil. Briefly stated, if God is responsible for designing not only the lovely parts of biology, but also the dangerous and nasty parts as well, then we have a theological problem on our hands. What kind of a God designs not only pretty flowers, but deadly malaria, too? Is God actually malicious? On the other hand, if God simply designed a process like Darwinism that He knew would lead to life, then, the thinking goes, He didn’t directly design those nasty parts of biology — the process did. So God escapes any blame for bad stuff.

The eminent geneticist and former priest Francisco Ayala says exactly that in so many words in his recent book, Darwin’s Gift to Science and Religion: Darwin’s “theory of evolution provided the solution to the remaining component of the problem of evil [that is, natural evil such as diseases and earthquakes].” (pp. 4-5) Ayala cannot stomach the alternative: “The natural world abounds in catastrophes, disasters, imperfections, dysfunctions, suffering, and cruelty.” (p. x)

I shudder in terror at the thought that some people of faith would implicitly attribute the calamity to the Creator’s faulty design.” (p. xi)

Attributing these to specific agency by the Creator amounts to blasphemy. Proponents and followers of ID are surely well-meaning people who do not intend such blasphemy, but this is how the matter appears to a biologist concerned that God not be slandered with the imputation of incompetent design. (p. 160)

Those are Ayala’s words, but as far as I can tell they reflect Miller’s sentiments too, who worries in his review that:

To Behe, these are not byproducts of a fruitful and creative natural world that also gave us the beauty of a sunset, the grace of an eagle, and the talent of a Beethoven. No, each vicious parasite and fatal disease is the direct and intentional work of the designer. This isn’t my conclusion; it’s Behe’s.

So there you have it. Miller (and Ayala) won’t tolerate life on earth being designed because that would impugn God’s reputation. Too many bad things inhabit the earth. They embrace Darwinism, at least in large part, for theological reasons.

Wow, and they say ID proponents get their conclusions from religious motives!

So, how to respond to such a position? The first thing to say is that it’s very hard to see how the Miller/Ayala position gets God off the hook. The “byproducts of a fruitful and creative [Darwinian] natural world” that Miller alludes to are not simply byproducts — they are deadly, dangerous, vicious byproducts. No matter if malaria were designed directly by God or indirectly by a sloppy process He put in motion, many children of mothers in malarious regions of Africa are going to be just as dead. There is going to be as much suffering in the world one way as the other.

Why couldn’t a grieving mother justifiably demand of an infinitely powerful God that He explain why He chose such a sloppy process to make life, instead of a more efficient process that would not produce natural evils such as parasites and tsunamis? One that wouldn’t cause such enormous pain? It seems to me that designing a poor Darwinian process that inevitably spins off natural evils leaves One as vulnerable to being sued for incompetence as directly designing them as finished products.

My own view (which Miller spectacularly fails to grasp) is that, as a scientist, one is obliged to look at the evidence of nature dispassionately and nonjudgmentally. If the coherence and complexity of the malaria parasite point to its purposeful design by an intelligent agent, then that’s where the data point. As a scientist, one is not allowed to pass judgment on the morality of nature. To reject the weight of evidence because it shows the universe to be something unpalatable is to betray science.

On the other hand, as a theist one can make an argument that what strikes us as evil in nature is part of a larger whole which is good. In his recent book Francisco Ayala wrote that one could regard tsunamis as the unintended side effect of a good process (plate tectonics) which is necessary to build a habitable world. Well, heck, one can make the same argument for parasites and viruses. It may well be that such seemingly vile creatures actually play positive roles in the economy of biology, of which we are in large part unaware. If that’s the case, then directly designing parasites and viruses is as defensible in terms of the overall goodness of nature as is designing the processes of plate tectonics. The fact that they are dangerous to humans is an unintended side effect of something that is good in itself.

What’s more, there can be just about as much real contingency and freedom in nature in the extended fine tuning view as in the view of theistic evolutionists of the Ayala/Miller stripe. Even if God purposely designed the malarial parasite, He may not have decreed that a particular infected mosquito would bite a particular person on a particular day, or that a particular tiger would eat some one in particular. In the case of the tiger (designed or not), for example, a human’s fate might depend on when he decides to go for a walk, which route he takes, etc., etc. Nature and human life would still be chockful of contingency and freedom.

As I wrote in The Edge of Evolution, it seems to me that our world was designed to be a a dangerous living stage, one that’s set up for improvisational theater. It allows for real suffering, real pleasure, real pain, real joy. It allows for real freedom and real consequences. But if the world were not designed in sufficient detail, then no intelligent life would be around to act on the stage.

25 October 2007

Kenneth R. Miller and the Problem of Evil, Part 2

Michael J Behe

(This is the second of three posts on Kenneth Miller and the problem of evil.)

Let me emphasize the last point of my previous post: Miller and I are only quibbling over the extent of design in the universe. Thefact of design, the principle of design, we agree on.

Now, let’s look a little closer at where Ken Miller draws the limits of design (the edge of evolution, one might say). Although they are clearly necessary, is there reason to suppose that the bare laws and constants of the universe — even if properly tuned — are sufficient to assure life occurs in our universe, as Miller supposes? The answer is no — many other features than just the bare laws of the universe have to be gotten right. I discuss this at considerable length in the last chapter of the book. But don’t just take my word for it. The prominent bioinformatician Eugene Koonin recently published a paper entitled “The cosmological model of eternal inflation and the transition from chance to biological evolution in the history of life”, (Biol Direct., 2007, 2:15). The gist of the paper is that — even given fine tuned laws and constants — the origin of life in our universe is so unlikely, that the non-theist Koonin invokes an infinite multiverse to assure that life happens somewhere.

I criticize such a multiverse view in the last chapter of The Edge of Evolution. But right here I want to contrast Koonin’s view with Miller’s. Koonin thinks that the bare laws and constants of the universe — fine tuned as they are — are still far from sufficient to assure an origin of life in our universe. Miller, however, without an argument, insinuates that they are. What does Miller know about the origin of life that Koonin doesn’t? Little, I’ll wager. So suppose Koonin is right that fine tuning the laws of the universe is far from sufficient to assure life. In that case, switching to Miller’s scenario, God would have set up a generic universe whose laws and constants were necessary for life, but not sufficient. Since many other conditions are required for life, Miller’s God likely made a fine tuned universe for naught. It would likely be a finely tuned universe that’s nonetheless barren of life.

In The Edge of Evolution I agree with Miller (and other “theistic evolutionists”) that the laws and constants of our universe are fine tuned, but argue that “fine-tuning” extends much more deeply into nature than previously supposed, and actually extends into life itself, at least down to the level of vertebrate class. I cleverly call this view “extended fine-tuning.” In the book I argue that any person who accepts a theistic evolutionary view, such as Miller does, should have no trouble in principle with the extended fine tuning view. It is, after all, just a matter of degree. In either case the designer fine tuned enough details of our universe to get intelligent life to arise.

But Miller viscerally opposes such an extended fine tuning view. His opposition strikes me as much stronger than the differences in our scientific positions should justify. I think the reason for his deep disdain of a relatively minor difference in our positions is not scientific. Rather, it’s theological.

24 October 2007

Kenneth R. Miller and the Problem of Evil, Part 1

Michael J Behe

(This is the first of three posts on Kenneth Miller and the problem of evil.)

Brown University biologist Kenneth R. Miller has penned a second review of The Edge of Evolution, this one for the Catholic magazine Commonweal (subscription required). In the new review Miller alludes to some scientific points from his first review inNature. (I refer readers to my previous rejoinder to that on this blog.) But much of the second review turns on the theological implications of the book.

In the new review Miller seems truly astounded that I argue that common descent is very strongly supported:

Those hoping that Behe would argue for a biblical version of human origins will be shocked. Indeed, Behe tells his readers that there must be “no relying on holy books or prophetic dreams,” and that it “would be silly” to treat the Bible “as some sort of scientific textbook.” Amen.

Gee, of all the folks in America who follow these issues, Miller must be the only person who doesn’t know that I most certainly do not “argue for a biblical version of human origins.” I take my data exclusively from the scientific observation of nature, not from religious sources. I have always thought the evidence for common descent is persuasive. I said so in Darwin’s Black Box over ten years ago; I’ve said so repeatedly in public and private, to intellectual friends and intellectual opponents. The only conclusion I can draw from Miller’s apparent shock is that, when it comes to intelligent design arguments, Ken Miller just doesn’t listen too well. He hears what he wants to hear from design arguments and then substitutes his own ideas when the actual statements of ID proponents don’t fit his mental script. Then he argues with great passion against a strawman.

So it seems Miller now belatedly realizes that he and I agree on common descent. (You’d think that would cheer him up a bit, but it sure doesn’t seem to in the review.) What’s more, we both believe the universe was designed, at least to a certain level. (You’d think that additional common ground would cheer Miller a bit too but, if so, he keeps it well disguised.)

Behe happily notes, as I would, that we live in a universe whose fundamental physical constants are remarkably hospitable to life. To me, and apparently to Behe, these constants may well reflect the will of a creator we would both identify as the God of Abraham.

So let me emphasize: Kenneth Miller is an intelligent design proponent. He believes that the laws of the universe were purposely set up to permit life to develop. Miller thinks that, to accomplish the goal of life, the universe had to be designed to the depth of its fundamental physical constants. I agree with him as far as he goes, but, on the other hand, as I write in The Edge of Evolution, I think design extends further into the universe, past physical constants, past anthropic coincidences, and well into biology. Yet, with respect to design, he and I differ only on degree, not on principle.

18 October 2007

Reply to Gross

Michael J Behe

The current edition of The New Criterion carries a lengthy reviewof The Edge of Evolution (subscription required) by the biochemist Paul Gross. Unfortunately, although he is commendably civil and kindly praises my writing and speaking abilities, Gross offers little of actual substance other than to declare the book’s arguments wrong. He quotes Ken Miller saying that the malaria calculations are wrong, and alludes to Sean Carroll’s declaration that, why, there is a vast number of (unspecified) papers showing how protein binding sites can evolve. For rejoinders to those claims, I refer readers to my comments on this blog concerning Carroll’s and Miller’s reviews.

17 October 2007

Back and forth with Sean Carroll in Science

Michael J Behe

Science has published a letter by myself responding to Sean Carroll’s earlier review of The Edge of Evolution. In my letter I note that:

In his unfavorable review of my book, The Edge of Evolution, Sean Carroll writes that “Behe’s chief error is minimizing the power of natural selection to act cumulatively,” and implies that I fail to discuss “pyrimethamine resistance in malarial parasites … –a notable omission given Behe’s extensive discussion of malarial drug resistance.

But, I demurred, I did write about pyrimethamine. Carroll admitted in Science right after my published letter that, well, yes, I did discuss pyrimethamine resistance, but his real concern was that I didn’t give it the spin he wanted:

Behe did indeed discuss pyrimethamine resistance on pages 75 and 76 of his book. My criticism is that Behe omitted the clear evidence for the cumulative selection of multiple changes in the drug target protein in nature and that he invoked an altogether different and unsupported explanation in an attempt to bolster his main premise.

Carroll’s beef is that several papers he cites (W. Sirawaraporn et al., Proc. Natl. Acad. Sci. U.S.A. 94, 1124 (1997); J. Yuvaniyama et al., Nat. Struct. Biol. 10, 357 (2003); C. I. Sandefur, J. M. Wooden, I. K. Quaye, W. Sirawaraporn, C. H. Sibley,Mol. Biochem. Parasitol. 154,1 (2007)) have shown that, in the laboratory, in some respects intermediate mutations in the enzyme-target of pyrimethamine have better activity than the wild-type enzyme. But this data proves too much. If the mutations improve the enzyme in vitro, then that begs the question of why organisms with these mutations don’t outcompete the wild type in nature, even in the absence of pyrimethamine.

One possibility, which plagues all in vitro work, is that perhaps the mutants have other, detrimental aspects, not measured in an assay, which makes the alteration a net burden in the wild. If that is the case, then the mutant enzyme might run rings around the wild-type enzyme when both are in a test tube in a lab, but could still be a bust in nature.

To see if a particular mutation in a particular enzyme helps an organism to survive in the wild, one has to show that it helps an organism to survive in the wild. None of the papers Carroll cites even tries to do that. On the other hand, the work I cite in my book looked at field studies of organisms in the wild. Workers wondered:

Because resistance to [pyrimethamine] can be conferred by a single point mutation, it was assumed that resistance could occur frequently. However, a recent population survey demonstrated a single origin of [resistant genes] in five countries: Thailand, Myanmar, PDR Lao, Cambodia, and Vietnam. (Hayton,K. and Su,X.Z. 2004. Genetic and biochemical aspects of drug resistance in malaria parasites. Curr. Drug Targets. Infect. Disord. 4:1-10)

It was hypothesized that multiple mutations in different genes might be required:

Because concurrent mutations in two different genes occur at reduced frequency, this would help explain the rarity with which resistance has evolved. (Nair,S., Williams,J.T., Brockman,A., Paiphun,L., Mayxay,M., Newton,P.N., Guthmann,J.P., Smithuis,F.M., Hien,T.T., White,N.J., Nosten,F., and Anderson,T.J. 2003. A selective sweep driven by pyrimethamine treatment in southeast asian malaria parasites. Mol. Biol. Evol.20:1526-1536)

(By the way, Hayton and Su 2004 also remark that, “Based on the mutant pfcrthaplotypes known so far, it is likely that simultaneous multipoint changes in pfcrtare necessary to confer [chloroquine resistance]”.)

Carroll implies I’m somehow less than honest for passing on the thinking of workers in the field in this area, while he passes off as near-conclusive ambiguous work done in vitro.

Toward the end of his lengthy letter Carroll remarks as an aside, “the complete disregard of a massive literature surrounding protein interactions [is] crucial to Behe’s entirely unfounded conclusion.” That’s rich, considering that Science cut out the final paragraph of my letter (Science allowed me about 200 words; they allowed Carroll about 500 words in response), which said:

Carroll writes [in his review], “it has been demonstrated that new protein interactions and protein networks can evolve fairly rapidly.” If he is implying the changes occurred by Darwinian means, “demonstrated” is question-begging. The references he cites [in his review] show only that differences exist in contemporary homologous protein sequences among various phyla, some functional, some not. How the functional differences arose — whether by random mutation and selection or not — is not addressed. On the other hand, studies I cite in my book show that, over thousands of generations, astronomical numbers of closely-studied microorganisms failed to develop new protein interactions or networks.

If there is a “massive literature” on the evolution of protein-protein interactions which is pertinent to the questions I raise, Sean Carroll somehow failed to cite any of it in his review.

15 October 2007

Korthof and Pseudogenes: Part 4

Michael J Behe

The Dutch biologist Gert Korthof maintains a website devoted to in-depth reviews of many books on evolution. Aside from often-insightful remarks, a delightful feature of his site is that he can write with great strength of feeling and yet not engage in insults or ad hominem remarks. He has posted an extensive review of The Edge of Evolution.

He makes two main points. First, that while I profess to believe in both common descent and intelligent design, he sees an internal contradiction — there cannot be, he thinks, common descent if there is intelligent design, and vice versa. The second point is that he thinks I contradict what I wrote in Darwin’s Black Box concerning the status of pseudogenes as evidence of common descent. I’ll take these points in turn.

Korthof writes:

The “designed group” contains at least Kingdoms, Phyla, Classes (and maybe Orders, Families and Genera). Behe’s “randomness group” contains at least species (and maybe genera, families and orders).

“Explicit design appears to reach into biology to a certain level, to the level of the vertebrate class, but not necessarily further” (p.220)

Apparently the vertebrate class is explicitly designed. That means that at a certain moment in the history of the earth the first vertebrate “was designed”. The fundamental problem here is that the reason for invoking design is that natural processes are not sufficient to produce vertebrates. However, as soon as one single nonnatural event is invoked during the history of life, the genetic continuity of life is broken. Common Descent is based on the vertical (sometimes horizontal) transmission of genetic information. Without that genetic continuity, Common Descent breaks down.

Korthof is incorrect here. As I read him, Korthof is saying that the first moment that some vertebrate class appeared was the moment that it was designed. Thus there is a discontinuity that can’t be classified as common descent. But as I tried to make clear especially in the last chapter of my book, all design might have been built into the initial conditions of the universe and unfolded over time. I try to get this point across with the figure of the überphysicist who selects a certain one out of very many universes which will develop in just the way he wishes; he “activates it”; and from there on everything follows according to unbroken natural law. It may be that in that universe there are some apparently amazing coincidences and astronomically low-probability events [which were front-loaded into the initial set-up], but all events follow without further prodding after the initial activation. Thus, contra Gert Korthof, there can indeed be purposeful intelligent design and common descent.

Concerning the second point — the status of pseudogenes, Korthof writes:

Here [in Darwin’s Black Box] Behe argues against Ken Miller. Miller claimed that Intelligent Design cannot explain pseudogenes of hemoglobin in humans, because it would mean that “the designer made serious errors, wasting millions of bases of DNA on a blueprint full of junk. Evolution can explain them as nothing more than failed experiments”. Indeed, it is true that in general one cannot conclude from structures with unknown function to no function at all, but the pseudogene is not an unknown structure, but a copy of a known functional gene with mutations which make it non-functional. So Behe’s critique fails. Behe’s second argument against pseudogenes as evidence for Common Descent is that “even if pseudogenes have no function, evolution has “explained” nothing about how pseudogenes arose” (DBB,226) and his third is that “these chance events do not mean that the initial biochemical systems were not designed.” (DBB,228).

My point is not to refute Behe’s arguments, but simply point out the amazing and extraordinary fact that Behe inDarwin’s Black Box dismissed exactly the same evidence that he now accepts without any explanation. In The Edgehe simply states “a broken hemoglobin gene” and forgets that he stated 10 years ago that “this argument is unconvincing for three reasons”. What was exactly wrong with his arguments in DBB?

This topic is actually pretty simple, but can get confusing if you take your eye off the ball. I take pseudogenes as good evidence of common descent, both in Darwin’s Black Box and The Edge. However, I do not take pseudogenes as evidence that random mutation and natural selection could have produced the original functioning gene which eventually gave rise to a pseudogene. Kenneth Miller was trying to argue that pseudogenes are positive evidence against all intelligent design. In my mind that’s like arguing that a broken down car is evidence against intelligent design. Miller’s argument was incorrect. But Korthof takes my rebuttal as arguing against common descent, which it wasn’t meant to do. It was an argument that pseudogenes do not speak to the ability of Darwinian processes to make functioning genes.

I think a lot of folks get confused because they think that all events have to be assigned en masse to either the category of chance or to that of design. I disagree. We live in a universe containing both real chance and real design. Chance events do happen (and can be useful historical markers of common descent), but they don’t explain the background elegance and functional complexity of nature. That required design.

12 October 2007

Microbe Magazine and the Bacterial Flagellum: Part 3

Michael J Behe

Dear Readers,

This is the third in a series of responses I’m posting this week.

In “Evolution of the Bacterial Flagellum” (Microbe Magazine, July 2007), Wong et al seek to counter arguments of intelligent design proponents such as myself that the flagellum did not evolve by random mutation and natural selection. Unfortunately, their otherwise-fine review misunderstands design reasoning and so fails to engage that issue. The critical passage from Wong et al is the first paragraph:

Proponents of the intelligent design (ID) explanation for how organisms developed claim that the bacterial flagellum (BF) is irreducibly complex. They argue that this structure is so complicated that it could not have emerged through random selection but had to be designed by an intelligent entity. One part of this claim is that each flagellar component is used solely for the purpose of making a flagellum that, in turn, is used only for motility. Further, each flagellar protein is assumed to have appeared independently of the other component proteins.

Although the first two sentences are correct, the last two sentences are quite wrong. (The authors cite no references for these latter claims.) It is no part of the design argument that each component of an irreducibly complex structure must be used solely for that purpose, nor that each part must arise independently. In my 1996 book Darwin’s Black Box, which brought the concept of irreducible complexity to wide public attention, I pointed out the fact that, for example, proteins of the blood clotting cascade share sequence homology with each other and with other serine proteases, and the fact that ciliary proteins such as tubulin are involved in other tasks in the cell. Yet I explained that neither sequence homology nor multiple functions showed how integrated systems containing many parts could be put together by small random steps. Unfortunately, Wong et al spend their efforts addressing their own erroneous assertions. They fail to address the only pertinent question, the question of whether random, unintelligent processes — even when filtered by natural selection — could plausibly build a structure such as the flagellum.

To address the adequacy of random processes plus selection would require rigorous experiments or calculations showing that the intricate, functional structures are not too improbable given the evolutionary resources available. Recent work bears negatively on this difficult question. In long term laboratory evolution experiments over tens of thousands of generations (Lenski, R.E. 2004. Phenotypic and genomic evolution during a 20,000-generation experiment with the bacterium Escherichia coliPlant Breeding Reviews 24:225-265), cultures of E. coli were repeatedly seen to lose the ability to make ribose and maltose, and to repair their DNA. Some mutations shut down expression of their flagellar genes, apparently to conserve energy. No selected mutations were observed which could plausibly be argued to be the incipient stages of some new, complex functional system. Similar kinds of results are seen in other well-studied evolutionary systems. For example, in response to strong pressure from the malarial parasite, the human genome has suffered a handful of positively-selected-yet-degradative mutations (Carter, R. and Mendis, K.N. 2002. Evolutionary and historical aspects of the burden of malaria. Clin. Microbiol. Rev. 15:564-594), including ones that render nonfunctional the genes for glucose-6-phosphate dehydrogenase, the alpha and beta chains of hemoglobin, band 3 protein, and others. Again, no selected mutations were observed which could plausibly be argued to be the incipient stages of some new, complex functional system.

To a skeptic such as myself, this does not look like the sort of process which could build complex molecular machinery.

11 October 2007

Science, E. coli, and the Edge of Evolution: Part 2

Michael J Behe

Dear Readers,

This is the second in a series of responses I’m posting this week, this one regardingthe Darwinian website The Panda’s Thumb,where a woman named Abbie Smith questioned whether results from HIV research actually square with the claims I made that little fundamental change has occurred in the virus, even though it attains enormous populations sizes and has a much increased mutation rate.

Although she calls herself a “pre-grad student,” the tone of the post is decidedly junior high, the tone of someone who is trying hard to compete with all the other Mean Girls on that unpleasant website. I’ll pass over all that and try to stick to the substance.

Her post mainly concerns a small protein coded for by HIV-1 called Vpu. She first points out that the amino acid identity between the homologous chimp SIV protein with HIV Vpu is 39%, much less than that of other homologous viral proteins, and she seems to regard that fact by itself as remarkable. Yet the alpha and beta chains of human hemoglobin are only about 44% identical, and have virtually superimposable structures and very similar functions. The fact that the chimp and human versions of VPU have 39% identity indicates they are structurally virtually identical. That doesn’t seem like a fundamental change to me.

She goes on to write that Vpu acts to degrade CD4 molecules by binding to them and recruiting the pathway that degrades CD4. Unfortunately, she seems not to have read the beginning of chapter 8 of The Edge of Evolution (“Objections to the Edge”), where I make some careful distinctions:

This chapter makes some important distinctions and addresses potential objections. It considers counter-arguments to my attempt to define the edge of evolution — not philosophical ones, about the “other side” of that boundary, but technical and logical ones about the line itself….

Another, more important point to note is that I’m considering just cellular proteins binding to other cellular proteins, not to foreign proteins. Foreign proteins injected into a cell by an invading virus or bacterium make up a different category. [emphasis added here] The foreign proteins of pathogens almost always are intended to cripple a cell in any way possible. Since there are so many more ways to break a machine than to improve it, this is the kind of task at which Darwinism excels. Like throwing a wad of chewing gum into a finely tuned machine, it’s relatively easy to clog a system — much easier than making the system in the first place. Destructive protein-protein binding is much easier to achieve by chance.

So the example she chose is from exactly the category that I excluded in the above paragraph. My exclusion isn’t arbitrary. As I wrote, there are many more ways to cripple a machine than to build one, so destructive Darwinian processes can appear to accomplish more. Yet The Edge of Evolution is concerned with how molecular machinery is constructed, not destroyed. One can’t ignore such critical distinctions and make progress. But, in my experience, many Darwinists overlook important differences.

She goes on to list several other properties of Vpu, but, while interesting, none at all are what one should call “fundamental” changes. For example, she notes, the HIV Vpu has several sites that are negatively charged by virtue of being phosphorylated. She continues, “Yet some SIVcpz Vpus have only one [phosphorylation] site, and instead utilize a simple string of negatively charged amino acids in place of the second site. Different ways of performing similar tricks with totally different amino acids. I think that’s biochemically significant as well.”

Well, I disagree. I don’t think that’s biochemically fundamental at all. In each case one has a blob of negative charge. Since the mutation rate of HIV is so extremely high, kinase sites are likely replaced every day in some virus with multiple glutamates or aspartates and vice versa. She also points out that some virus Vpu subtypes have altered the location of modification sites or acquired signals to localize protein in particular subcellular compartments. But again, because of the virus’s extremely high mutation rate, such sites would be expected to come and go frequently. As I emphasized in The Edge of Evolution, HIV’s enormous numbers and very high mutation rate cause immense variation. The question, however, is to what extent the immense variation has produced novel virus systems or machinery? And, as I indicated, the answer is very little. Butler at al (HIV Genetic Diversity: Biological and Public Health Consequences, Current HIV Research, 2007, 23-45) remark under the subheading “Biological Consquences of HIV Diversity”:

With such breadth of genetic diversity among HIVs, one might expect significant biological differences between the clades. Although interesting variations can be seen, much of the data concerning biological implications of HIV diversity is contradictory.

Plenty of differences do exist, and some are “interesting”, but not all that great.

Darwinists overlook the considerable power of the example of the relatively minor changes in HIV: there have been a truly astronomical number of copies produced in just the past fifty years or so. And because of its much increased mutation rate, it has undergone in the past half century as many of some kinds of mutations as all the cells have undergone in the history of the world. If Darwinism had the power that its boosters claim, we should expect to see truly fundamental changes. Yet despite the enormous number of opportunities, only minor changes have appeared. That is very strong evidence of the strict limits on what Darwinian processes can accomplish.

9 October 2007

Science, E. coli, and the Edge of Evolution: Part 1

Michael J Behe

Dear Readers,

As I wrote in The Edge of Evolution, Darwinism is a multifaceted theory, and to properly evaluate the theory one has to be very careful not to confuse its different aspects. Unfortunately, stories in the news and on the internet regularly confuse the facets of Darwinism, ignore distinctions made in The Edge of Evolution, or misstate the arguments of intelligent design. The disregard for critical distinctions blurs the issues badly. Over the next few days I will briefly respond to four separate stories
1) A few months ago an interesting paper in Science“Adaptive mutations in bacteria: high rate and small effects”, by the group of Isabel Gordo demonstrated that beneficial mutations in E. coli were more frequent than had been thought. In fact, the authors remark that “We found a rate on the order of 10(-5) per genome per generation, which is 1000 times as high as previous estimates, and a mean selective advantage of 1%.” They show that the previous underestimates of the beneficial mutation rates were likely due to clonal interference — accumulation of beneficial mutations in large bacterial populations which then interfere with each other to dominate the population, making beneficial mutations seem less frequent. Does this new result mean that Darwinian evolution can construct molecular machinery much easier than thought?
No. While the result is interesting, readers of The Edge of Evolution will not be very surprised by it. As I showed for mutations that help in the human fight against malaria, many beneficial mutations actually are the result of breaking or degradinga gene. Since there are so many ways to break or degrade a gene, those sorts of beneficial mutations can happen relatively quickly. For example, there are hundreds of different mutations that degrade an enzyme abbreviated G6PD, which actually confers some resistance to malaria. Those certainly are beneficial in the circumstances. The big problem for evolution, however, is not to degrade genes (Darwinian random mutations can do that very well!) but to make the coherent, constructive changes needed to build new systems. The bottom line is that the beneficial mutations reported in the new Science paper most likely are degradatory mutations, and so don’t address the challenges outlined in The Edge of Evolution.