Rarely does the public catch a glimpse of how Darwinists actually behave toward colleagues who disagree with their view of biological origins. Thus, as a public service, I’m presenting here a correspondence, initiated by Darwinists and unsolicited by our side, that provides readers of this blog with such a glimpse. Briefly, a Johns Hopkins biologist named David Levin sent an unsolicited and wonderfully insulting letter to Michael Behe (the entire letter is given toward the bottom of this post). Levin also attached a pdf of a Nature article (see the very bottom of this post). As it is, Levin copied Ken Miller, Richard Dawkins, and the usual suspects. Ken Miller, thinking that Levin had a slam-dunk against ID, then suggested to Levin that he also send me what he had sent Behe (presumably to crush my spirits). Here, then, is the exchange. To trace the chronology, you’ll need to start from the bottom and work your way up. I post Mike Behe’s response to Levin with Mike’s permission. After Behe’s response and my second response to Levin, we never heard from him again.
—– Original Message —–
Date: Thu, 22 Feb 2007 23:36:44 -0600
To: “David E. Levin”
From: “William A. Dembski”
Subject: Re: Fw: Evolution of a biochemical pathway by gene duplication and specialization
Cc: richard.dawkins AT zoo.ox.ac.uk, robison AT nucleus.harvard, aorr AT mail.rochester, rdoolittle AT ucsd, Kenneth_Miller AT Brown, lziska AT asrr.arsusda, Lisa West , Behe
Dear Dr. Levin,
I receive many unsolicited emails asking me to comment on how the theory of intelligent design deals with this or that objection to it. You are asking me to respond to an informal letter that you wrote to Michael Behe sketching out some worries you have about his notion of irreducible complexity. Let me suggest you write up your thoughts in a formal article and submit them to a peer-reviewed publication. Once it’s accepted, I’ll be happy to look at it more closely and offer comment. As it is, Michael Behe was gracious enough to send you some comment on your letter (I’ve pasted his comments below for continuity), though he appears much less impressed with your work than you are.
In your note to me below you write: “you seem incapable or unwilling to discuss the data or the inescapable conclusion that emerges from them.” Actually I’m quite willing. If you would like me to speak at your campus on the topic of intelligent design and address your data, I can put you in touch with my speakers bureau.
Best wishes,
Bill Dembski
—– Original Message —–
At 09:26 AM 2/22/2007, David E. Levin wrote:
Dr. Dembski,
You seem to have missed the point of my letter to Behe. It was not to bring to his attention the Kellis et al. paper. That was merely the starting point, the prerequisite understanding from which my work followed. It did not escape my notice that you had nothing whatever to say about my demonstration of how a real biochemical pathway has evolved to a more complex state. Perhaps all the biochemistry and genetics is beyond you.
Still, your criticism of the Kellis et al. paper was telling. Lets see, you asserted that it is now three years old, as though its age as some bearing on the validity of its conclusions. You clued into the phrases computational algorithm and statistical analysis as though such things invalidate any conclusions the authors might derive. These guys sequenced and assembled the genome of a species and aligned its eight chromosomes with the 16 chromosomes of another species. Yes, they used computers and statistics to assist them in their analysis. Its a 10 megabase eukaryotic genome! You sort of need computers and statistics to crunch all that information.
Whats important here is to look at the remarkable picture that emerges from this work. A species ancestral to the bakers’ yeast underwent a whole-genome duplication, followed by loss of most of the duplicated genes. This is how bakers’ yeast arrived at current genomic organization. As I said before, there is no other way to interpret these data. But you seem incapable or unwilling to discuss the data or the inescapable conclusion that emerges from them. I am taken aback by the extreme level of intellectual dishonesty that pervades the intelligent design circle. Your tactic is always to deflect and misdirect. Never mind the data, its old, or it uses statistics, or it presupposes common descent. Why are you so afraid of the data? Its as though you creationists have closed your eyes, covered your ears with your hands and are muttering to yourselves My mind is made up, dont confuse me with facts.
As for your assertion that nonteleological evolutionary mechanisms are not sufficient to drive the evolutionary process, I have provided an excellent example of precisely how this happens. Deal with it!
David E. Levin, Ph. D.
Professor
Dept. of Biochem. & Molec. Biol.
Johns Hopkins Bloomberg School of Public Health
615 N. Wolfe St.
Baltimore, MD 21205
Ph. (410) 955-snip
fax (410) 955-snip
—– Original Message —–
At 01:26 PM 2/22/2007, Michael Behe wrote:
Hello, Professor Levin, nice to meet you. Well, I see that even though you work in Baltimore, you’ve managed to avoid acquiring any Southern charm. Most folks consider it rude to send insulting, unsolicited mail to people you’ve never met, even if you don’t like their views. I hope at least you are polite toward people who agree with you.
Thanks for sending me the brief report on your work. Clearly you are excited about it, so I hope you don’t mind that I find it unimpressive even if your interpretation of events is correct. Here’s how I see your scenario: Roughly a hundred million years ago the ancestor of S. cerevisiae had a well-regulated, multicomponent pathway, including a prodigy protein, Mpk1, that had several activities. That complex pathway is taken by you for granted, as an unexplained starting point. Then the genome duplicated. In one of the duplicated copies of the prodigy protein a point mutation caused it to lose one of its pre-existing abilities. In the other copy of the prodigy protein, although it hasn’t happened yet in nature, you have in your own lab demonstrated that, by golly, a simple mutation can cause the other pre-existing ability to be lost too. I’m afraid I find all of that unsurprising. It has been known for quite a long time that mutations can inactivate protein functions.
The single gain of function in your whole story is the new binding site for Rlm1. That, however, is a comparably modest change; since the consensus binding sequence for MADS-box proteins is about ten nucleotides, with considerable redundancy, such a sequence would be expected to occur by chance perhaps every ten kilobases or so, and either to have been present in some segment of the population at the time of the genome duplication, or to be produced by point mutation very shortly thereafter. Such sites are thought to be gained and lost continually. At the very best then, assuming that modern Mpk1 eventually does lose the ability to activate SBF, according to your own scenario we are left with yeast that does pretty much the same thing with two very similar pathways that its ancestor did with one. And that meager (potential) result required enormous evolutionary resources: a hundred million years, whole genome duplication, and huge numbers of yeast likely many orders of magnitude more than the numbers of a vertebrate species that would be available in a similar span of time.
Frankly, I’m puzzled why that is supposed to be an example of the power of Darwinian processes. Id be happy to cite it myself as an illustration of genome drift within tight limits set by severe constraints. The trivial changes the scenario involves would be expected to have been available in the yeast population a very short time after the initial genome duplication event. Yet here we are twiddling our thumbs, tens of millions of years later, still waiting for the scenario to complete itself. This suggests to me that your scenario is overlooking many complicating factors, such straightforward issues as whether genome duplications or gain/loss of regulatory binding sites or loss of protein function even in a duplicated copy are deleterious, and whether there are useful functions close by existing functions. Such questions plague any simplistic Darwinian scenario, including the ones you cite that were proposed for the blood clotting cascade, but it seems few people are willing to take the difficulties seriously.
I wish you well with your work, Professor Levin. But please don’t write to me again unless you can restrain your childish sneers.
Sincerely,
Mike Behe
P.S. – I apologize for bothering all the people who were copied by Professor Levin on his original email.
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