RationalWiki:Kitzmiller v. Dover annotated transcript/P039

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THE COURT: Good morning to all. Mr. Muise, if it's Tuesday, we must be on the blood clotting.

MR. MUISE: We will be getting to blood clotting, immunity systems, and many more complex systems, Your Honor.

THE COURT: All right. You may proceed.

MR. MUISE: Thank you.

(Whereupon, Michael Behe, Ph.D., resumed the stand and testimony continued.)

DIRECT EXAMINATION (CONTINUED)

BY MR. MUISE:

Q. Good morning, Dr. Behe.

A. Good morning.

Q. Before we do get to the blood clotting, I need to circle back to sort of cover one housekeeping matter.

MR. MUISE: If I may approach the witness, Your Honor?

THE COURT: Yes.

BY MR. MUISE:

Q. Sir, I've handed you what has been marked as Defendants' Exhibit No. 237, which is an article from Saier, correct?

A. That's right.

Q. Is that one of the articles that you referenced during your testimony and appeared on one of the slides regarding the type III secretory system?

A. Yes, it is.

Q. Okay. Thank you, sir. Sir, yesterday, just to sort of recap and bring us to where we need to begin this morning, I had asked you if some scientists had argued that there is experimental evidence that complex biochemical systems can arise by Darwinian processes, and I believe you indicated there were two that are offered, correct?

A. That's right.

Q. And the first one was the lac operon?

A. Yes.

Q. And we discussed that yesterday?

A. Yes.

Q. And what is the second one?

A. The second one concerns what's called the blood clotting cascade, the system for clotting blood in animals. And I should say that, emphasize again that this is the second example of an experimentally -- an experimental result that was offered as evidence against some of the arguments that I made in Darwin's Black Box.

In this one, this is directed more to the question of irreducible complexity than to the question of whether Darwinian processes can put together a complex system.

Q. Now, sir, we've put up on the slide a figure, 6-5, that appears on page 142 in the Pandas text. Can you explain what we see here?

A. That's right. This is an electron micrograph of some red blood cells caught in a meshwork of a protein called fibrin, which forms a blood clot. And most people, when they think about blood clotting, if they think about it at all, it appears to be a simple process.

When somebody cuts themself, a minor cut slows down, stops, and heals over, and it doesn't seem like -- it doesn't seem like much at all. But thorough investigation over the past 40 to 50 years has shown that the blood clotting system is a very intricate biochemical system. And I believe there's an illustration of it on the next slide.

Q. Now you referred to, I believe, a blood clotting cascade, is that correct?

A. That's right.

Q. Can you explain a little bit to us as you're explaining what we see here on this particular diagram?

A. Okay, sure. Yeah, this is a figure of the blood clotting cascade taken from the biochemistry textbook by Voet and Voet, which is widely used in colleges and universities around the country. You see all these names of things and arrows. The names of things are very complex proteins of the complexity or sometimes more complex than the hemoglobin that I showed yesterday.

In blood clotting, the material that forms the clot cannot, of course, be in its solid clotted form during the normal -- during the normal life of an animal or all of the blood would be clotted, and that would be inconsistent with its life. So the material of the clot that actual eventually forms the clot exists as something called fibrinogen, which is actually a soluble pre-cursor to the clot material.

It floats around in your bloodstream during normal times. But when a cut occurs, fibrinogen is transformed into something called fibrin, and that happens when another protein comes along and cuts off a small piece of fibrinogen, a specific piece which exposes a sticky site on it, sticky in the sense of those two proteins yesterday that I saw that -- that I showed you that had complimentary surfaces.

It exposes a sticky site on the surface of the fibrinogen, which allows the many copies of fibrinogen, now turned into fibrin, to aggregate and stick to each other, forming the blood clot.

But what is the component that cuts fibrinogen and activates it? Well, the component is another protein called thrombin. But now we've got the same problem again. If thrombin were going around cutting fibrinogen and turning it into fibrin, all the blood would clot, and that would congeal the blood and kill the animal.

So thrombin itself is an inactive form called prothrombin, so it has to be activated when a cut occurs. And that's the responsibility of another protein. And that protein exists in an inactive form, and it's -- the activation of that is the responsibility of another protein.

So in the blood -- it's called a blood clotting cascade because one component acts on the next which acts on the next which acts on the next and so on. Now notice that the blood clotting cascade actually has what are called two branches. There is one in this box up here is labeled the intrinsic pathway. And this is labeled the extrinsic pathway. So there are actually two branches to this blood clotting cascade.

Q. I believe this section is addressed in the textbook Pandas, correct?

A. Yeah, that's correct. On the left is a figure from Of Pandas and People illustrating the blood clotting cascade. And that was drawn after the illustration from the textbook by Voet and Voet. On the right-hand side is the illustration for the blood clotting cascade that appears in Darwin's Black Box.

I discussed the blood clotting cascade in one chapter of that -- of my book, and the illustration is very similar to the one in Pandas.

Q. I believe the diagram in Pandas is found on page 143?

A. Yes, that's right.

Q. Now these two diagrams, the one that appears in Darwin's Black Box and one of the blood clotting cascade appear, to my eye, to be virtually similar or almost exactly similar?

A. Yeah, they are very similar, except for the color in Pandas and so on. And that's because I wrote the discussion in Pandas and, of course, also in my own book. So the figures are very similar between the two.

Q. Now you testified yesterday that you coined the term irreducible complexity in Darwin's Black Box, which was published in 1996, is that correct?

A. Yes.

Q. So that book was published actually three years after Pandas was written, is that accurate?

A. Yes, that's correct.

Q. Is it accurate to say then that the concept of irreducible complexity was not fully developed when you had written that section in Pandas on blood clotting in 1993?

A. Yes, that's right. I was still contemplating the idea.

Q. Does Pandas, however, discuss the complexity of this system, the blood clotting system?

A. Yes, it does. It elucidates all the parts of the system.

Q. Is that discussion consistent with your discussion in Darwin's Black Box?

A. Yes, it introduces the concept of the purposeful arrangement of parts and says that's how we perceive design.

Q. That's introduced in the Pandas book?

A. Yes, uh-huh.

Q. When you talk about the purposeful arrangement of parts, that's similar to what you were discussing yesterday in your testimony, is that correct?

A. Yes.

Q. So is the scientific explanation of the blood clotting system similar to the -- the discussion in Pandas similar to the blood clotting cascade scientific explanation in Darwin's Black Box?

A. That's right, they're essentially the same. I think it's more detailed in Darwin's Black Box.

Q. In fact, you did use the similar diagrams?

A. Yes, that's correct.

Q. To explain the two?

A. Yes, uh-huh.

Q. I believe the next slide we have is, this is from your -- you discussed this and treated this as well in your book Debating Design, is that correct?

A. That's right. When I wrote Darwin's Black Box, and when Darwin's Black Box was subsequently reviewed by people, some of them looked at the argument about the blood clotting cascade and argued against what I had written in Darwin's Black Box.

And I thought that the counterarguments were themselves flawed, and so I answered some of those arguments in a variety of cites, but most recently in the chapter in that book, Debating Design, published by Cambridge University Press from the year 2004.

I wrote The Blood Clotting Cascade. Having dealt with some common misconceptions about intelligent design, I will examine two systems that were proposed as serious counterexamples of my claim of irreducible complexity. One of them discussed in that article is the blood clotting cascade.

Q. If you could then, explain to us how you refute the claims that are made that the blood clotting cascade is experimental evidence to refute irreducible complexity?

A. Okay. In the next slide, I believe that shows an excerpt from an article written by a man named Russell Doolittle entitled A Delicate Balance, which appeared in a publication called the Boston Review in 1997. Now Russell Doolittle is a very eminent scientist, a professor of biochemistry at the University of California, San Diego.

He's a member of the National Academy of Sciences, and has worked on the blood clotting system for the past 45 years or so. And this article was a part of the symposium organized by Boston Review, which again is published by MIT, and contained contributions from a number of academics, scientists discussing my book and discussing a book that had been recently published by Richard Dawkins of Oxford University.

Participants included myself, Russell Doolittle, James Shapiro, who is a professor of microbiology at the University of Chicago, Alan Orr, who is a professor of evolutionary biology at the University of Rochester, Robert DiSilvestro, who is a professor of biochemistry at Ohio State, and a number of other people as well.

And in his essay, Professor Doolittle argued that, in fact, there was experimental evidence showing that the blood clotting system was not irreducibly complex. And he said the following. Let me read the quote. Quote, Recently the gene for plaminogen (sic) -- and that's actually a typo. There should be an S there. The gene for plaminogen (sic) was knocked out of mice -- which means that it was destroyed by molecular biological methods -- and predictable, those mice had thrombotic complications because fibrin clots could not be cleared away.

Let me stop a second and explain that plasminogen is a protein that acts as a chemical scissors which cuts up and removes blood clots once the clot has finished its job. Let me resume the quote from Russell Doolittle. Not long after that, the same workers knocked out the gene for fibrinogen in another line of mice. Again, predictably, these mice were ailing, although in this case, hemorrhage was the problem.

Let me stop again and explain that fibrinogen, remind you, is the pre-cursor of the clot material itself, the pre-cursor of those fibers. And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal.

Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra. So Professor Doolittle's point, if I just might briefly say, was that, if you knock out one component of the blood clotting cascade, yes, those mice have problems.

If you knock out a different component in a different line of mice, yes, those mice have problems, too. But if you make a string of mice in which both of those components were missing, then the mice are normal and the blood clotting cascade is okay. And so presumably then, that shows that the blood clotting cascade is not irreducibly complex.

Q. Was there a particular study that Professor Doolittle is referring to?

A. Yes, it's shown on the next slide. This is the article that he was referencing in his own essay. It's entitled Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency. Now if we could go to the next slide.

Now because of the phrase, rescues mice, in the title, Professor Doolittle thought that the mice missing both components were normal. But it turns out, that was a misreading of the article.

In the abstract of the article itself, the authors write, quote, Mice deficient in plasminogen and fibrinogen are phenotypically indistinguishable from fibrinogen deficient mice. Now translated that into English on the next slide.

That means that mice missing both components have all the problems that mice missing fibrinogen only have. Their blood does not clot. They hemorrhage. Female mice die during pregnancy. They are not normal. They are not promising evolutionary intermediates. So if we look at this table of the symptoms of the various strings of mice, we can see what the authors meant by that phrase, rescues mice.

Lacking plasminogen, mice can't remove blood clots once their job is done and their blood circulation gets interfered with and they develop problems such as thrombosis, ulcers, and so on. Lacking fibrinogen, they can't clot blood in the first place, and they have a different suite of symptoms.

When they lack both, they have been rescued from the symptoms of plasminogen deficiency, but only to suffer the symptoms of fibrinogen deficiency. And if you think about it for just a minute, it's easy to understand what is going on. When an animal lacks plasminogen, it can't remove blood clots and its circulation becomes impeded and it suffers problems.

Lacking fibrinogen, it can't make clots in the first place, and so hemorrhage is a problem. Lacking both, it doesn't matter that it's lacking plasminogen, because the plasminogen's job is to remove blood clots after the job is finished. But the mouse missing both components can't form clots in the first place. So there are no clots to remove.

Q. Has subsequent work verified those results?

A. Yes, here's a table of not only the work that was cited in this discussion here on plasminogen fibrinogen, but also subsequent work by the same group of scientists who knocked out other components of the blood clotting cascade, including something called prothrombin and something else called tissue factor.

And if you look at the -- under the column labeled effect, in each case the blood clotting cascade is broken. They suffer hemorrhage. They cannot clot their blood. And that is exactly the result you would expect if, in fact, the blood clotting cascade were irreducibly complex, as I had written.

Q. So Professor Doolittle's refutation of your claims was based on a misreading of the study, is that correct?

A. That's right. He misread the original paper that he pointed to. And if I could make a couple of points based on this. As I said, this study, or this essay by Professor Doolittle and the one I discussed yesterday by Professor Miller were the two examples which offered experimental evidence that either irreducible complexity was not correct or that random mutation and natural selection could explain complex biochemical systems.

But if you look at the exact studies that were offered as support for Darwinian evolution, and you look at them closely, in reality, they highlight the difficulties for Darwinian evolution. So I think this is an illustration of how a scientist's preconceptions about the truth of a theory or the validity of a theory can affect his reading of the evidence.

And one more point is that, Professor Doolittle, of course, is a very eminent scientist. Professor Miller is, too. And they're quite capable of surveying the entire scientific literature for studies that they think are problems for my argument for intelligent design.

And nonetheless, when they surveyed the whole literature, and they seemed to be motivated to look for counterexamples to intelligent design, when they do so, they offer studies such as this, which are, at best, very problematic and none of which, I would say, are arguments against intelligent design.

So in my mind, I conclude that since highly motivated capable scientists who could advance arguments or who could point to studies that have created problems for intelligent design, that they have failed to do so, makes me confident that intelligent design is a good explanation.

Q. Now these article findings, the actual findings in these articles, is that what you would expect to find for an irreducibly complex system?

A. Yes, that's right. This is completely consistent with my expectations.

Q. As far as you know, has Professor Doolittle ever acknowledged that he misread that paper?

A. Yes, he has.

Q. And if I could --

MR ROTHSCHILD: Objection. Hearsay, Your Honor. I would move to strike.

MR. MUISE: Your Honor, he just -- he has an understanding that Professor Doolittle has indicated he has misread this paper.

MR ROTHSCHILD: If he has a basis, I'd like to see it.

THE COURT: Well, it's his understanding, and I'm take it for that. I won't take it as a matter of fact. His understanding is, he didn't quote something that Professor Doolittle said. It's simply, I'll take it as his understanding, and you're free to cross-examine him and present rebuttal evidence, if you see fit. So it's overruled.

BY MR. MUISE:

Q. Dr. Behe, I'd ask you to look at the exhibit binder that I had provided you yesterday. It's at your table in front of you. If you go to tab 17, please.

A. Yes.

Q. You'll see an exhibit marked Defendants' Exhibit 272. Is that the article by Russell Doolittle that you've been referring to here in your testimony?

A. Yes, that's correct. This is a web version.

MR ROTHSCHILD: Objection, Your Honor. I want to make clear, I think that's not the acknowledgment of the mistake, it's just the article that's being referred to. I just want to clarify that.

MR. MUISE: I think the question was pretty clear.

BY MR. MUISE:

Q. That's the article in the Boston Review that you're referring to?

A. Yes, this is Russell Doolittle's article in the Boston Review.

THE COURT: Does that resolve the objection?

MR ROTHSCHILD: Yes. I just want to clarify, this was not Dr. Doolittle's acknowledgment of a mistake.

THE WITNESS: Yes.

THE COURT: All right.

BY MR. MUISE:

Q. Dr. Behe, does anyone else know how the blood clotting cascade can be explained in Darwinian fashion and other proposed examples or explanations?

A. No, that's one of the very nice things about science is that, if there is no explanation in the science library in scientific literature, and if leaders in the field do not know how something could have come about, and presumably they know the literature very, very well, then one can be confident that not only do they not know how something could have been done, but nobody else in the world knows how that could have been done as well. And that's important to keep in mind because some people claim that nonetheless.

Q. And that's my next question. There have been individuals that nonetheless have made such claims, and do you have some slides to bring that up?

A. Yes, that's correct. On the next slide is an excerpt from an article by a man named Michael Ruse. Michael Ruse is a professor of philosophy of science currently at Florida State University. And in particular, he's a philosopher interested in Darwinian thought.

And he's written many books on Darwin, his ideas, the history around them, and so on. And several years after my book came out in 1998, Professor Ruse wrote an article entitled Answering the Creationists, Where They Go Wrong and What They're Afraid Of, and had it published in a magazine called Free Inquiry. And he said the following in the article.

Quote, For example, Behe is a real scientist, but this case for the impossibility of a small-step natural origin of biological complexity has been trampled upon contemptuously by the scientists working in the field. They think his grasp of the pertinent science is weak and his knowledge of the literature curiously, although ventsly, outdated.

For example, far from the evolution of clotting being a mystery, the past three decades of work by Russell Doolittle and others has thrown significant light on the ways in which clotting came into being. More than this, it can be shown that the clotting mechanism does not have to be a one-step phenomenon with everything already in place and functioning. One step in the cascade involves fibrinogen, required for clotting, and another, plaminogen -- there's that typo, missing the S -- required for clearing clots away.

And he goes on in his article to quote that passage from Russell Doolittle's Boston Review essay that I showed on the slide a couple slides ago. So this excerpt, in my view, shows that Professor Ruse relies completely on Professor Doolittle's explanation for the blood clotting cascade and has no independent knowledge of his own.

As a matter of fact, the fact that the same typo, the same misspelling of plasminogen occurs in Professor Ruse's essay makes me think that he relied on Professor Doolittle even for the spelling of the components of the cascade. So the point is that, even though Professor Ruse is a prominent academic concerned with Darwin and Darwinian thought, he has no knowledge that Professor Doolittle does not have concerning the blood clotting cascade.

Q. Do you have another example, sir?

A. Yes, another person has written on this, a man named Neil Greenspan, who is a professor of pathology at Case Western Reserve University, and he wrote an article in a magazine called The Scientist in the year 2002 entitled Not-so-intelligent Design. In the article, he writes the following. Quote, The Design advocates also ignore the accumulating examples of the reducibility of biological systems. As Russell Doolittle has noted in commenting on the writings of one ID advocate -- and perhaps I can be forgiven if I think he means me -- mice genetically altered so they lack either thrombin or fibrinogen have the expected abnormal hemostatic phenotypes. However, when the separate knockout mice are bred, the double knockouts apparently have normal hemostasis, reducible complexity after all, at least in the laboratory.

So the reasoning here exactly mimics the reasoning of Russell Doolittle in his Boston Review article. And let me just point out here that he talks about thrombin or fibrinogen, but the study was actually on plasminogen and fibrinogen. So again, I think this illustrates that even a scientist has -- even a scientist writing publicly on this topic, even a scientist writing publicly on this topic in order to argue against intelligent design has no more knowledge of this than Professor Doolittle has.

And once more, I think this speaks to the point of how firmly a theory can guide persons' thinking. I think the fact that Professor Ruse relied so heavily on Professor Doolittle, and Professor Greenspan did, too, and apparently they did not even go back and read the article on blood clotting that was being disputed, shows that they are so confident in Darwinian evolution that they don't think they have to, you know, check the facts.

They can rely on the authority of a person like Professor Doolittle. So I think that shows the grip of a theory on many people's thinking.

Q. Do you have an additional example?

A. Yes, one other excerpt here. In 1999, the National Academy of Sciences issued a booklet called Science and Creationism. And in it, they write the following, quote, The evolution of complex molecular systems can occur in several ways. Natural selection can bring together parts of a system for one function at one time, and then at a later time, recombine those parts with other systems of components to produce a system that has a different function.

Genes can be duplicated, altered, and then amplified through natural selection. The complex biochemical cascade resulting in blood clotting has been explained in this fashion.

Let me make a comment on this. Professor Doolittle is a member of the National Academy of Sciences. There is no other member of the National Academy who knows anything more about blood clotting than Professor Doolittle. But if Professor Doolittle does not know how Darwinian processes could have produced the blood clotting cascade, as I think is evident from his pointing to an inappropriate paper in his attempt to refute a challenge to Darwinian evolution, then nobody in the National Academy knows either. I should also -- well, I'll --

Q. Do they cite any papers or experiments to support this claim, the National Academy of Sciences, in this particular booklet?

A. No. That's a very interesting point. They simply assert this. They do not cite any paper in any journal to support this. And it's an interesting point, if I may say so. I've heard said earlier in this trial that not every utterance by a scientist is a scientific statement.

And that's something that I entirely agree with. And it's also true that not every utterance by a scientist even on science is a scientific statement. And it's also true that not even, not every proclamation, or not every declaration by a group of scientists about science is a scientific statement.

Scientific statements have to rely on physical evidence. They have to be backed up by studies. And simply saying that something is so does not make it so. In fact, this statement of the National Academy is simply an assertion. It is not a scientific statement.

Q. Does the National Academy of Sciences, in this document that you referenced, give any other examples of complex biochemical systems that have been explained?

A. This is the only example that they point to.

Q. In his testimony, Dr. Miller has pointed to the work of, I believe, you pronounce is Jiang, J-i-a-n-g --

A. Yes.

Q. -- and Doolittle and Davidson, et al, to argue against the irreducible complexity of the blood clotting system. Do you agree with his assessment of those studies?

A. No, I do not.

Q. And you have some diagrams to explain this further, sir?

A. Yes, I do. This is a slide from Professor Miller's presentation showing work from Jiang and Doolittle. And he also shows a diagram of the blood clotting cascade. And notice again, it's a branched pathway with the intrinsic pathway and the extrinsic pathway.

And Professor Miller makes the point that in DNA sequencing studies of something called a puffer fish, where the entire DNA of its genome was sequenced, and scientists looked for genes that might code for the first couple components of the intrinsic pathway, they were not found.

And so Professor Miller demonstrated that by -- if you could push to start the animation -- Professor Miller demonstrated that by having those three components blanked out in white. Nonetheless, puffer fish have a functioning clotting system. And so Professor Miller argued that this is evidence against irreducible complexity.

But I disagree. And the reason I disagree is that I made some careful distinctions in Darwin's Black Box. I was very careful to specify exactly what I was talking about, and Professor Miller was not as careful in interpreting it.

In Darwin's Black Box, in the chapter on blood clotting cascade, I write that, a different difference is that the control pathway for blood clotting splits in two. Potentially then, there are two possible ways to trigger clotting. The relative importance of the two pathways in living organisms is still rather murky. Many experiments on blood clotting are hard to do. And I go on to explain why they must be murky.

And then I continue on the next slide. Because of that uncertainty, I said, let's, leaving aside the system before the fork in the pathway, where some details are less well-known, the blood clotting system fits the definition of irreducible complexity.

And I noted that the components of the system beyond the fork in the pathway are fibrinogen, prothrombin, Stuart factor, and proaccelerin. So I was focusing on a particular part of the pathway, as I tried to make clear in Darwin's Black Box.

If we could go to the next slide. Those components that I was focusing on are down here at the lower parts of the pathway. And I also circled here, for illustration, the extrinsic pathway. It turns out that the pathway can be activated by either one of two directions. And so I concentrated on the parts that were close to the common point after the fork.

So if you could, I think, advance one slide. If you concentrate on those components, a number of those components are ones which have been experimentally knocked out such as fibrinogen, prothrombin, and tissue factor.

And if we go to the next slide, I have red arrows pointing to those components. And you see that they all fall in the area of the blood clotting cascade that I was specifically restricting my arguments to. And if you knock out those components, in fact, the blood clotting cascade is broken. So my discussion of irreducible complexity was, I tried to be precise, and my argument, my argument is experimentally supported.

Q. Now just by way of analogy to maybe help explain further. Would this be similar to, for example, a light having two switches, and the blood clotting system that you focus on would be the light, and these extrinsic and intrinsic pathways would be two separate switches to turn on the system?

A. That's right. You might have two switches. If one switch was broke, you could still use the other one. So, yes, that's a good analogy.

Q. So Dr. Miller is focusing on the light switch, and you were focusing on the light?

A. Pretty much, yes.

Q. I believe we have another slide that Dr. Miller used, I guess, to support his claim, which you have some difficulties with, is that correct?

A. Yes, that's right. Professor Miller showed these two figures from Davidson, et al, and from Jiang, et al, Jiang and Doolittle, and said that the suggestions can be tested by detailed analysis of the clotting pathway components.

But what I want to point out is that whenever you see branching diagrams like this, especially that have little names that you can't recognize on them, one is talking about sequence comparisons, protein sequence comparisons, or DNA nucleotide sequence comparisons. As I indicated in my testimony yesterday, such sequence comparisons simply don't speak to the question of whether random mutation and natural selection can build a system.

For example, as I said yesterday, the sequences of the proteins in the type III secretory system and the bacterial flagellum are all well-known, but people still can't figure out how such a thing could have been put together. The sequences of many components of the blood clotting cascade have been available for a while and were available to Russell Doolittle when he wrote his essay in the Boston Review.

And they were still unhelpful in trying to figure out how Darwinian pathways could put together a complex system. And as we cited yesterday, in Professor Padian's expert statement, he indicates that molecular sequence data simply can't tell what an ancestral state was. He thinks fossil evidence is required.

So my general point is that, while such data is interesting, and while such data to a non-expert in the field might look like it may explain something, if it's asserted to explain something, nonetheless, such data is irrelevant to the question of whether the Darwinian mechanism of random mutation and natural selection can explain complex systems.

Q. So is it your opinion then, the blood clotting cascade is irreducibly complex?

A. Yes, it is.

Q. Now Professor Pennock had testified that he was co-author on a study pertaining to the evolution of complex features. Does this study refute the claim of irreducible complexity?

A. No, it does not.

Q. And I believe we put up a slide indicating the paper that was apparently by Lenski and Pennock, correct?

A. That's right. Richard Lenski, and Professor Pennock was co-author, and several other co-authors as well. This is the first page of that article. Let me reemphasize that the last two systems that I talked about, the lac operon and the blood clotting cascade were ones in which experiments were done on real biological organisms to try to argue against intelligent design and irreducible complexity.

This study of Lenski is a computer study, a theoretical study not using live organisms, one which is conducted by writing a computer program and looking at the results of the computer program.

If I could have the next slide. This is an excerpt from the abstract of that paper. Let me read parts of it. It says, quote, A long-standing challenge to evolutionary theory has been whether it can explain the origin of complex organismal features, close quote. Let me just stop there to emphasize that these workers admit that this has been a long-standing problem of evolutionary theory.

MR ROTHSCHILD: Objection. This mischaracterizes the document.

THE COURT: Elaborate on that objection.

MR ROTHSCHILD: I'm sorry?

THE COURT: Elaborate on the objection. You say he's mischaracterizing --

MR ROTHSCHILD: This is a long-standing challenge not a long-standing problem.

THE COURT: Well, I think he's characterizing something and not necessarily reading from it. What are you objecting to?

MR ROTHSCHILD: I think he's mischaracterizing it. That's my objection.

THE COURT: Again, you'll have him on cross. This is direct examination. I'll overrule the objection. You may proceed.

BY MR. MUISE:

Q. Dr. Behe, just for reference, the article you are referring to is published in 2003, is that correct?

A. That's correct, yes.

Q. Continue, please.

A. So apparently, this had not been explained up until at least the publication of this paper. The authors continue, quote, We examined this issue using digital organisms, computer programs that self-replicate, mutate, compete and evolve. Let me close quotes there.

You have to remember that the labeling of these things as organisms is just a word. These things are not flesh and blood. These things are little computer programs. There are strings of instructions. And a comparison of these to real organisms is kind of like comparing an animated character in some movie to a real organism.

So the authors go on. And the next slide, please. And this is the first figure on the first page of their article. And I just want to emphasize, this is just an illustration emphasizing that these -- there are computer instructions. Each one of these are little computer instructions; swap, nand, nand, shift R. They have no similarity to biological features, biological processes. You see over here little strings of ones and zeroes.

These are characters in a computer memory. These are not anything biological. Let me say that, theoretical studies of biology can oftentimes be very useful. And I'm certainly not denigrating the use of computer in studying biology. But one has to be careful, very careful that one's model, computer model mimics as closely as possible a real biological situation. Otherwise, the results one obtains really don't tell you anything about real biology.

And I think that the Lenski paper, it does not mimic biology in the necessary way. And that's shown on the next slide.

Q. Let me just, to clarify. So a crucial question is whether or not it's a good model for biological process, is that correct?

A. Yes, that's right.

Q. And you don't believe this is one?

A. No, I think it misses the point and it assumes what should be proven instead. And let me try to explain that with an excerpt from the article itself. The authors write in their discussion, quote, Some readers might suggest that we stacked the deck by studying the evolution of a complex feature that could be built on simpler functions that were also useful, close quote.

Let me stop there to comment that, yes, that is exactly what I would suggest, that they stacked the deck. They built a model in which there was a continuous pathway of functional Features very close together in probability, which is exactly the question that's under dispute in real biological organisms. Is there such a pathway in real biological organisms?

So to assume that in your computer model is stacking the deck. Let me go back to the abstract. They continue, quote, However, that is precisely what evolutionary theory requires. Now I'll close quote there, and let me comment on that.

Just because your theory requires something does not mean it exists in nature. James Clerk Maxwell's theory required ether. Ether does not exist. So just because a theory requires it is no justification for saying that building a model shows something about biology.

Q. Dr. Behe, if you could, just so we're clear on the record, because I'm not sure if we have it that clear, can you identify the title and the specifics of this article, so we're clear on what specific article you're referring to?

A. Yes, this is an article by Lenski, Ofria, Pennock, and Adami published in the year 2003. The title is The Evolutionary Origin of Complex Features published in the journal Nature, volume 423, pages 139 to 144.

Q. Thank you. And the authors go on to say in their discussion, indeed, our experiments showed that the complex feature never evolved when simpler functions were not rewarded. This is not surprising to me. This shows the difficulty of irreducible complexity. If you do not have those closely stacked functional states, if you have to change a couple things at once before you get a selectable property, then I have been at pains to explain, that's when Darwinian theory starts to fail, not when you have things close together.

And to build them into your model is, again, begging the question. The fact that when they do not build that into their model, they run into problems that complex features then don't evolve. That is exactly what I would expect. I would cite this as evidence supporting my own views.

Q. Have other scientists made similar criticisms?

A. Yes. A couple years ago, there was an article published by two scientists named Barton and Zuidema published in a journal called Current Biology. The title of the article is Evolution, The Erratic Path Towards Complexity.

And much of the article is a commentary on the work by Lenski and co-workers. And if I could just read a couple excerpts from that article. They make a couple interesting points. The authors say, complex systems, systems whose function requires many interdependent parts, that is irreducible complexity systems in my view, are vanishingly unlikely to arise purely by chance.

Darwin's explanation of their origin is that natural selection establishes a series of variants, each of which increases fitness. This is an efficient way of sifting through an enormous number of possibilities, provided there is a sequence of ever-increasing fitness that leads to the desired feature, close quote.

So that's the exact -- that's the big question. Is there such a pathway, or is it, as it certainly appears, that one has to make large numbers of changes before one goes from a functional selectable state to a second functional selectable state? And Barton and Zuidema continue in their discussion.

They say, in Lenski's artificial organisms, the mutation rate per site is quite high. So, in other words, if I might make my own comment, they are using -- they are using factors which are not common for biological organisms.

Now picking up with the paper again. So that favorable pairs can be picked up by selection at an appreciable rate. This would be unlikely in most real organisms because, in these, mutation rates at each locus are low. In other words, again, they are building into the model exactly the features they need to get the result they want.

But building it into your model does not show that that's what exists in nature. And Barton and Zuidema comment further, quote, Artificial life models such as Lenski, et al's, are perhaps interesting in themselves, but as biologists, we are concerned here with the question of what artificial life can tell us about real organisms.

It's -- it can be productive and it can be interesting to do such studies as Lenski, et al, did. But the big question is, do they tell us anything about real organisms? And I am very skeptical that this study does so.

Q. Now have you done some work yourself that's somewhat similar?

A. Yes, indeed. A year ago, as I mentioned earlier in my testimony, David Snoke and myself published a paper in the journal Protein Science entitled Simulating Evolution by Gene Duplication of Protein Features that Require Multiple Amino Acid Residues.

In this, we also -- it was essentially a theoretical study using computer programs to try to mimic what we thought would occur in biology. But we tried, as closely as possible, to mimic features of real proteins and real mutation rates that the professional literature led us to believe were the proper reasonable values.

And when we used those values, the short, the gist of the matter is that, once -- if there is not a continuous pathway, if one has to make two or three or four amino acid changes, those little changes from that figure of two interacting proteins that I talked about yesterday, if one has to make several changes at once, then the likelihood of that occurring goes -- drops sharply in the length of time, and the number of organisms in a population that one would need to have that goes up sharply.

Q. Would it be fair to say that your model is closer to biological reality?

A. Well, I certainly think so.

Q. Now Dr. Miller testified that the immune system is being explained by Darwinian theory. Do you agree with that?

A. No, I do not.

Q. And so I'd ask you if you could explain why not?

A. Yes. On the next slide is a -- is the first slide of Professor Miller's discussion of this topic and his presentation simply showing a model of an immunoglobulin protein. And here is kind of a little cartoon version of the same thing, the immunoglobulin protein.

He goes on the next slide to take an excerpt from my book where in a chapter where I discussed the immune system and argue that, in fact, it is not well-explained by Darwinian processes but, in fact, is better explained by design.

Q. Can you explain that Sisyphus reference?

A. Yeah, okay. Sisyphus. I said, Sisyphus himself would pity us. That was just a literary flourish there. Sisyphus is a figure from mythology who was doomed for eternity to have to roll a bolder up a hill, and whenever he got to the top of the hill, the bolder would roll back, and he would have to start all over again.

This was meant to indicate frustration. And I argued that Darwinian attempts at explanations would be similarly frustrating.

Q. I just want to make a point clear. You said there were two examples where those who claim that irreducible complexity does not work or is not a valid explanation, they use experimental evidence, and that was the blood clotting system and the lac operon. How does the immunity system, is that experimental evidence or is that a theoretical claim?

A. No, this is mostly a theoretical claim. There is no experimental evidence to show that natural selection could have produced the immune system. And I think that's a good example of the different views that people with different theoretical frameworks bring to the table.

If we could show the next slide. Professor Miller shows this slide from a reference that he cited by Kapitonov and Jurka, and he has titled Summary, Between 1996 and 2005, each element of the transposon hypothesis has been confirmed. He has this over this diagram.

But again, as I mentioned previously, whenever you see diagrams like this, we're talking about sequence data, comparison of protein, sequences, or gene sequences between organisms. And such data simply can't speak to the question of whether random mutation and natural selection produced the complex systems that we're talking about.

So Professor Miller -- so, in my view, this data does not even touch on the question. And yet Professor Miller offers as compelling evidence. And one more time, I view this as the difference between two people with two different expectations, two different theoretical frameworks, how they view the same data.

And I'd like to take a little bit of time to explain why such studies do not impress me. And I'll do so by looking at one of the papers that Professor Doolittle -- I'm sorry, Professor Miller, that's his name, cited in his presentation, Kapitonov and Jurka, that was published this year.

I just want to go through, and just kind of as a quick way to show why I am not persuaded by these types of studies. I want to excerpt some sentences from this study to show what I consider to be the speculative nature of such studies.

For example, in this excerpt, the authors say, something indicates that they may be important. This may indicate. It may be encoded. It might have been added. If so, it might have been derived. Alternatively, it might have been derived from a separate unknown transposon. It was probably lost. And we have a lot more of those, one more slide at least.

It says, we cannot exclude the possibility. In any case, the origin appears to be a culmination of earlier evolutionary processes. If so, this might have been altered. Again, without going into the detail of the article, I just wanted to emphasize those phrases to point out what I consider to be the very speculative nature of such papers.

Here's what I view to be the problem. The sequence of the proteins are there. The sequence of the genes are experimentally determined. And the question is, what do we make of that information? People like Professor Miller and the authors of this paper working from a Darwinian framework simply fit that data into their framework.

But to me, that data does not support their framework. It does not offer experimental evidence for that framework. They're simply assuming a background of Darwinian random mutation and natural selection and explaining it -- or fitting it into that framework, but they're not offering support for it.

Q. Dr. Behe, is there another paper that scientists point to for the support that the immune system can be explained by this Darwinian process?

A. Yes, there is. There is one more that I have to discuss. Here is a recent paper, again the year 2005, by Klein and Nikolaidis entitled The Descent of the Antibody-Based Immune System by Gradual Evolution. And on the next slide is an excerpt from the initial part of their discussion where they say, quote, According to a currently popular view, the Big Bang hypothesis, the adaptive immune system arose suddenly, within a relatively short time interval, in association with the postulated two rounds of genome-wide duplications.

So these people, Klein and Nikolaidis, are going to argue against what is the currently popular view among immunologists and people who study the immune system on how that system arose.

Q. And what is the Big Bang hypothesis that's referred to here?

A. Well, that's kind of a label that they put on to kind of indicate the fact that the immune system appears in one branch of animals, the vertebrates, and any obvious pre-cursors or functional parts of such a system do not appear to be obvious in other branches of animals.

So it seems like the immune system arose almost complete in conjunction with the branching of vertebrates from invertebrate.

Q. Do scientists acknowledge that or treat that as a problem for Darwin's theory?

A. Well, in my experience, no, nobody treats such a thing as a problem for Darwin's theory.

Q. Do you consider it a problem?

A. I certainly consider it a problem. But other scientists who think that Darwinian evolution simply is true don't consider much of anything to be a problem for their theory.

Q. Why do you consider it a problem?

A. Because the -- as Darwin insisted, he insisted that adaptations had to arise by numerous successive slight modifications in a very gradual fashion. And this seems to go against the very gradual nature of his view.

Q. Now has this paper been held up by scientists as refuting claims against intelligent design?

A. Yes, it has. As a matter of fact, Professor Miller cited it in his expert report, although he didn't refer to it in his testimony. Additionally, I attended a meeting on evolution at Penn State in the summer of 2004 where one of the authors, Juan Kline, spoke on his work, and he interpreted it in those terms.

Q. Now we have some quotes, I believe, from this paper that you want to highlight?

A. Yes. Again, I want to pull out some excerpts from that paper just to show you why I regard this as speculative and unpersuasive. For example, they start with, by saying, quote, Here, we sketch out some of the changes and speculate how they may have come about. We argue that the origin only appears to be sudden. They talk about something as probably genuine.

It probably evolved. Probably would require a few substitutions. It might have the potential of signaling. It seems to possess. The motifs presumably needed. One can imagine that a limited number. It might have been relatively minor. Quote, The kind of experimental molecular evolution should nevertheless shed light on events that would otherwise remain hopelessly in the realm of mere speculation. They're talking about experiments that have yet to be done.

Next slide, I have even more such quotations. These factors are probably genuine. Nonetheless. They might have postdated. Nevertheless. Albeit. It seems. This might have been. These might represent. They might have been needed. This might have functioned. This might have. And this might have contributed.

So again, this is just a shorthand way of trying to convey that, when I read papers like this, I do not see any support for Darwin's theory. I read them as speculative and -- but nonetheless, people who already do believe in Darwin's theory fit them into their own framework.

Q. Now Dr. Miller cited numerous papers in his testimony to support his claims on irreducible complexity, the type III secretory system, and so forth. Have you done a review of those papers and have some comments on them that you prepared slides for?

A. Yes, I did. I went through many of the papers that Professor Miller cited, as many as I could, and simply, as a shorthand way of trying to indicate or trying to convey why I don't regard any of them as persuasive, I simply did a search for the phrases, random mutation, which is abbreviated here in this column, RM, and the phrase, natural selection.

Random mutation, of course, and natural selection are the two elements of the Darwinian mechanism. That is what is at issue here. And so this is, you know, this is, of course, a crude and perhaps shorthand way, but nonetheless, I think this illustrates why I do not find any of these papers persuasive.

When I go through the papers that Professor Miller cited on the blood clotting cascade, Semba, et al, Robinson, et al, Jiang and Doolittle, there are no references to those phrases, random mutation and natural selection.

Q. Some of your indications on this slide, you have 0 with asterisks and some without. Is there a reason for that?

A. Yes. The papers that have asterisks, I scanned by eye. I read through them visually. Ones that do not have an asterisk, I was able to do a computer search for those phrases because they are on the web or in computer readable form. I have a number of other such tables.

On the next one are references that Professor Miller cited on the immune system. And again, none of these references contain either those phrases, random mutation and natural selection. There were a couple more references on the immune system that Professor Miller cited, and they didn't contain those phrases either.

In references for the bacterial flagellum and the type III secretory system, there was one paper by Hauch, a review in 1998 that did use the phrase natural selection. However, that phrase did not occur in the body of the paper. It was in the title of one of the references that Hauck listed.

And on the next slide, I think there are papers cited by Professor Miller on common descent of hemoglobin. And again, those phrases are not there. I think there's another slide or two, if I'm not mistaken. This is the one on what he described as molecular trees, Fitch and Margoliash, from 1967. And I didn't find the phrase there either. So again, this is a shorthand way of showing why I actually considered these off-the-point and unpersuasive.

Q. So all these papers that are being used to provide evidence for Darwin's theory of evolution, in particular, the mechanism evolution of natural selection, yet they don't mention random mutation or natural selection in the body of the works?

A. That's correct.

Q. Could you summarize the point then, Dr. Behe, that you are making with, referring to these studies and the comments you made about the speculative nature of some of these studies?

A. Yes. Again, much of these studies, in my view, are speculative. They assume a Darwinian framework. They do not demonstrate it. And certainly, you know, certainly scientists should be free to speculate whatever they want. You know, science usually starts with speculation, but it can't end with speculation.

And a person or, and especially a student, should be able to recognize and differentiate between speculation and actual data that actually supports a theory.

Q. So it would be beneficial to point this sort of feature that you just described, point that out to students?

A. I very much think so.

MR. MUISE: Your Honor, we're going to be moving again into another subject, and it appears to be close to the time for a break.

THE COURT: Yeah, why don't we take a break at this point. I think that makes good sense. We'll break for 20 minutes at this juncture, and we'll return and pick up direct examination at that point.

(Whereupon, a recess was taken at 10:11 a.m. and proceedings reconvened at 10:36 a.m.)

recess
THE COURT: All right. Mr. Muise, you may continue.

MR. MUISE: Thank you, Your Honor.

BY MR. MUISE:

Q. Dr. Behe, Dr. Miller severely criticized Pandas for its treatment of the topic of protein sequence similarity. Do you agree with his assessment?

A. No, I don't.

Q. And I would ask you to explain why not?

A. On the next slide, we see one of Professor Miller's slides, the first, I think, in his sequence where he very severely criticized the book Of Pandas and People for its treatment of the question of why similar proteins in separate organisms have the differences in their sequence that they do.

And on the next slide, this is again a slide from Professor Miller. He reproduces a figure from Pandas which shows -- it's hard to read on here -- that the difference in the number of amino acids of a protein called cytochrome c, which is a small protein which is involved in energy metabolism and which has about 100 amino acids in it, the difference between that protein which occurs in fish is about 13 percent.

About 13 amino acids differ between the fish cytochrome C and frog cytochrome C; and about 13 or so between bird and fish cytochrome C; and about 13 between mammalian cytochrome C and fish cytochrome C. So that remarkably, the proteins in these different organisms all seem to have roughly the same number of differences, although the differences are not the same differences, but they have the same number of differences from fish cytochrome C.

And Pandas discusses this in their text. And Professor Miller -- Professor Miller takes Pandas to task because he says that, in fact, this is a well-studied and a problem that has been solved by evolutionary theory. For example, he says, in fact, these sequence differences confirm that each of these organisms is equi-distant from a common ancestor, which is the actual prediction of evolutionary theory.

He has a little tree diagram there, too. But one has to realize that, in fact, Professor Miller is mistaken. Evolutionary theory does not predict that. Or one could say, evolutionary theory predicts that in the same sense that evolutionary theory predicted that the vertebrate embryos, as drawn by Haeckle, should be very, very similar to it; or the prediction of evolutionary theory after newer results came out, that vertebrate embryos could vary by quite a bit; or the prediction of evolutionary theory that the type III secretory system would be a good pre-cursor for the flagellum; or the prediction of evolutionary theory that the flagellum -- or that the type III secretory system might be derived easily from a flagellum.

So, in fact, what we have, I will try to make clear, is an instance where experimental science comes up with data, and the data is attempted to be fit into a framework. But this data was not predicted by any evolutionary theory.

Q. How was Pandas' treatment of this compared with what Dr. Miller found?

A. In my view, Pandas' treatment of this topic is actually much more accurate than Professor Miller's discussion of the same topic in his testimony here. Professor Miller, in his discussion, where he says that, evolutionary theory predicts this remarkable amount of difference, is referring to something, although he does not call it such, something called the molecular clock hypothesis.

And notice that, in fact, in Pandas, on the page opposite to the figure that Professor Miller used in his presentation, there is a section entitled A Molecular Clock where they go through and discuss some issues with it, which I will talk about later on.

Q. Just to be clear for the record, the diagram, figure 9 that you've been referring to that Dr. Miller cited in his testimony, appears on page 38 of Pandas, is that correct?

A. Yes.

Q. And the discussion of the molecular clock appearing on the subsequent page appears on page 39 of Pandas, as indicated in this slide, is that correct?

A. That's correct.

Q. Do you have some slides and discussion as to how this molecular clock problem is treated in the science community?

A. Yes, I do, and it will probably take about 10 minutes or so to go through it. So please be patient. But here is a cover of the Biochemistry textbook that I referred to frequently here by Voet and Voet, which is used in many universities and colleges across the country.

And they have a section on the molecular clock hypothesis and on cytochrome C in which they discuss these issues. Let's imagine -- I'm going to try to explain a molecular clock. Let's imagine that these lengths of time -- these lines represent time. And down at the bottom of the screen is a time -- a distant time ago, and up at the top is modern time.

And the branches here represent events in the course of life where a population of organisms split into two -- split into two, and one branch went off to form one group of organisms and another group went off to form a different type of organisms.

Q. If I might just interrupt briefly. You're referring to a phylogenetic tree that has vertical lines that branch off to each other, and that's what you're referring to the vertical lines running, two at the top of the diagram, and then they branch off into different sections?

A. That's correct. That's exactly right.

Q. Could you continue, please?

A. Yes. So, for example, at this branch, a population of organisms split off that went on to become plants, and at this branch, a population split off which went on to become animals.

Now I suppose that before any split in the population, the pre-cursor population organisms had a cytochrome c with a certain sequence. We'll say there was a hundred letters. Just think of a string of a hundred letters; Z, Q, A, L, W.

Now, however, when we get to this branch point, we have a group of organisms going off to form the animals, another going off to form the plants. They no longer interbreed, and so that string of a hundred letters representing cytochrome c can't accumulate mutations in it separately.

So, for example, suppose once every year or so, the cytochrome c in the branch that is forming the plants suffered a mutation, so that one of those letters changed from what it had been. And similarly, in the branch going off to form the animals, once every hundred years or so, one of those letters changed into something.

Not necessarily the same. Maybe a different one. So that after a while, those two sequences would be different. And suppose every hundred years, that happened, one change, one change, one change, and so on. After a while, you'd start to accumulate a number of changes.

Now further suppose that along the line to animals, the population of animals split into two, one line leading to, say, insects, and another line leading to mammals. Now you could have the same thing with the cytochrome c sequence that had been mutating all along, but now they split into two populations, and now these two populations also begin to accumulate mutations independently.

But notice here, they start right at the branch point with the same sequence. But after, say, a hundred years, this will have one difference with what it had at the beginning. This one will have one difference, too. And they don't necessarily have to be the same difference.

So they'll start to accumulate differences with each other between, say, the branch leading to the insects and the branch leading to the mammals. Now here's the point. Any sequence along this branch should have accumulated the same number of sequences between any sequence on this branch.

So that the number of differences between insects and plants should be roughly the same between, as that between mammals and plants. Any animal and any plants should have roughly the same number of differences. Whereas between subgroups of animals that have split off from each other earlier than animals did from plants, they will have had less time to accumulate differences in their amino acid sequences. And so they will have -- so they will have fewer differences.

Q. You mean, if they split off later. You said, earlier. They were split off later, correct?

A. Thank you. Yes, later. So Professor Miller has, I believe, this sort of model in mind, which is commonly -- which is a common way of thinking of these things in science.

So the idea is that, since fish branched off from those other groups of vertebrates, mammals, birds, and so on, the fish, under this model, would be expected to have the same number of differences in their amino acid sequences between themselves and all those other vertebrate groups.

Q. So here you have plants splitting off at the same time as the insects or you have the same -- you have the same connection between insects and plants as plants and mammals?

A. That's right. So the critical point is that, the difference between animals, any animal group like mammals and plants and insects and plants, they should have the same difference between animals and plants, no matter what the subgroup of animals.

But between animals which branch off -- groups of animals which branched off at an earlier -- or from each other earlier to the current time, they would have less time to accumulate differences. And I believe this is what Professor Miller had in mind.

However, this model has some difficulties with it which are well recognized and have been discussed in the literature for over 40 years. For example, I said, suppose every hundred years or so, a mutation occurred. Okay. Well, suppose that in this branch, every hundred years or so, a mutation occurred. But in this branch, suppose a mutation occurred every 50 years.

And suppose when these split, the mutation rate again changed somewhat. Now you would not expect this nice, neat pattern to occur. Now you would expect a jumble. It's not quite clear what one might expect. And it turns out, that's a real problem because it's thought that most mutations accumulate in a lineage when an organism reproduces.

When an organism reproduces, the DNA in it has to be replicated, and that gives a chance for mutations to come into the DNA. But different organisms can reproduce at greatly differing rates. For example, a fruit fly might have a generation time of two weeks, and an elephant might have a generation time of 20 years.

So if the number of mutations that a protein or gene underwent was proportional to the number of generations, you might expect a lineage with quickly reproducing organisms to accumulate mutations much more quickly, and the one with slowly reproducing organisms to accumulate more slowly.

And I believe this is -- on the next slide, there shows discussion from the Biochemistry textbook explaining exactly that point. Let me quote from it. Quote, Amino acid substitutions in a protein mostly result from single base changes in the gene specifying the protein. If such point mutations mainly occur as a consequence of errors in the DNA duplication process, then the rate at which a given protein accumulates mutations would be constant with respect to numbers of cell generations.

Not with time. With numbers of cell generations. If, however, the mutations process results from a random chemical degradation of DNA, then the mutation rate would be constant with absolute time. So here's this complication. If most mutations occur during replication, you wouldn't expect this difference that we see in cytochrome c.

If, for some reason, mutations occurred constant with time, well, then you might expect that. But the problem is, we know of no reason why that necessarily -- that has to be so, why a mutations have to -- would have to occur constant in time.

Q. Is there a problem in addition to this generational rate change?

A. Yes, that's one complication, but there's another one as well. And that's that, this so-called molecular clock seems to tick at different rates in different proteins. And this is an illustration again from the Biochemistry textbook that applies to this point.

On the bottom, the X axis, this is time. This is 200 million, 400 million, a billion years, and so on. This is number of -- or percent amino acid sequence difference. And the idea is that, here's the line for cytochrome c.

Organisms which diverge about 200 million years ago have these many sequence differences; about 400 million years ago, have these many, and so on. Look at how nice and neat that is. However, for another protein, hemoglobin, the molecular clock seems to tick faster. For the same amount of time, hemoglobin has maybe twice as many mutations.

Another region of a protein called a fibrinopeptide seems to accumulate mutations extremely rapidly. And a fourth protein, if you can look at the bottom of the figure, it's hard to see, for something called histone H4, barely accumulates any mutations at all. Organisms in very widely separated categories have virtually identical histone H4's.

Now to resolve this problem, it was postulated that perhaps this has to do with the number of amino acid residues in a protein that are critical for its function. Perhaps in some proteins, you know, most of the amino acid residues cannot be changed or it destroys the function and would destroy the organism.

And in others, maybe some can be changed, but not others. And so you can change those. And perhaps in another group, almost all of them can be changed without really affecting the function. And so that's an interesting idea. But there are also difficulties with that because, under that model, you would predict that if you changed the amino acid sequence of histone H4, then that should cause problems for an organism, because all of its, or most of its, or practically all of its amino acids are critical for function. But experimentally, that is not supported, as shown on the next slide.

Q. Is this -- so you've done work in this area with the histone H4 and the molecular clock?

A. Yes, uh-huh. I've written this commentary in 1990 in a journal called Trends in Biochemical Sciences, commenting on the work of somebody else who experimentally took an organism called yeast into the lab and altered its histone H4 and actually chopped off a couple amino acids at the beginning portion of that protein.

And when he looked, it seems that it didn't make any difference to the organism. The organism grew just as well without those mutations, which is surprising, which is not what you would expect if all of those residues were critical for the function of that protein, histone H4.

Later on, in the year 1996, I and a student of mine, Sema Agarwal, we were interested in this problem of histone H4 and molecular clock, and so we experimentally altered some amino acid residues into protein and changed them into different amino acids, with the expectation that these might destroy the function of the protein. But it turned out not to.

These positions, these amino acids could be substituted just fine, which is unexpected, and which kind of complicates our interpretation of the molecular clock hypothesis. So there are two complications; complications upon complications.

One, we would expect the number of mutations to accumulate with generation time, but it seems to accumulate, for some unknown reason, with absolute time. And the second is that, proteins accumulate mutations at different rates. We would expect that it would have to do with how vulnerable they are to mutations, and mutations might destroy the function of one protein that evolved slowly, but that is not experimentally supported.

Q. Now has this problem been discussed in the scientific literature?

A. Yes, this has been continuously discussed ever since the idea of the molecular clock hypothesis was first proposed in the early 1960's by two men named Emile Zuckerkandl and Linus Pauling. And here are a couple of papers which deal with the difficulties of the molecular clock hypothesis.

Here's a recent one, Gillooly, et al, published in the Proceedings in the National Academy of Sciences, entitled The Rate of DNA Evolution, Effects of Body Size and Temperature on the Molecular Clock. In this publication, they say that, in fact, the size of an organism and temperature can affect how fast or how slow this clock might tick.

Francisco Ayala has written on this frequently. Here's one from 1997. And I should say, Francisco Ayala is a very prominent evolutionary biologist. He wrote an article in 1997 entitled Vagaries of the Molecular Clock. And I think the title gets across the idea that there are questions with this hypothesis.

And in 1993, a researcher named Tomoka Ohta published an article in the Proceedings of the National Academy of Sciences entitled An Examination of the Generation-time Effect on Molecular Evolution in which she considers exactly that complication that the textbook Voet and Voet pointed out, this generation-time effect.

You know, why shouldn't organisms that reproduce more quickly accumulate more mutations. I have another slide just from one more recent paper. This paper by Drummond, et al, is entitled Why Highly Expressed Proteins Evolve Slowly. And it's referring to the sequence evolution that I've been discussing.

It was published in the Proceedings of the National Academy of Sciences, and this was from an online version. This is so recent that I don't think it has yet appeared in print. The point I want to make with this is that, these people treat this question as a currently live question.

They start off by saying, a central problem in molecular evolution is why proteins evolve at different rates. So that question I was trying to illustrate with histone H4, why does one protein tick faster and another one tick more slowly, that's still -- that is still unknown.

And I think I will skip the rest of this slide and go to the next slide and just point out a couple words here. Drummond, et al, say, Surprisingly, the best indicator of a protein's relative evolutionary rate is the expression level of the encoding gene.

The only point I want to make with this is that, they are reporting what is a surprise, what was not expected, which was not known, you know, 40 years ago, which has only been seen relatively recently. And they say, quote, We introduce a previously unexplored hypothesis, close quote.

And the point I want to emphasize is that, here in this paper published, you know, weeks ago, that they are exploring new hypotheses to try to understand why proteins have the sequences that they do.

Q. So in summary, this protein sequence, the fact that the equi-distant from a common ancestor is not what evolutionary theory would actually predict?

A. That's right. Evolutionary theory makes no firm prediction about this anymore than it makes a firm prediction about the structure of vertebrate embryos.

Q. It's a common understood problem that biologists are trying to resolve at this point?

A. Yes, within the community of scientists who work on this. People have been working on it for decades.

Q. Is this a problem that an American Biology teacher should be aware of?

A. Yes, an American Biology teacher should be aware of it, because an article on this very topic was published in the magazine, American Biology Teacher, a couple years ago, which is put out by the National Association of Biology Teachers.

And the article is entitled Current Status of the Molecular Clock Hypothesis. And one of the first -- this is a red arrow that I added to the figure. One of the first subsections of the article is entitled How Valid is the Molecular Clock Hypothesis? And if you'll advance to the next slide, let me just read the last line from the paper.

The author says, The validity of a molecular clock, except in closely related species, still remains controversial. So the point is that, extrapolating across wide biological distances, such as from fish to other vertebrates, that is controversial.

Maybe similar species, species of mice or some such thing, okay. But when you try to extrapolate further, the model is quite controversial.

Q. How does Pandas then address this issue?

A. Well, I have here the section from Pandas entitled The Molecular Clock where they discuss exactly all these things. They discuss the molecular clock, the standard molecular clock model, the naive molecular clock model, and then they discuss complications with it.

Let me just read this section from Pandas on the molecular clock. They write, quote, Some scientists have suggested that the idea of a molecular clock solves the mystery. The explanation they advance is that there is a uniform rate of mutation over time, so quite naturally, species that branched off from a common ancestor at the same time in the past will now have the same degree of divergence in their molecular sequences.

There are some serious shortcomings, however, with this explanation. First, mutation rates are thought to relate to generation times, with the mutation rates for various molecules being the same for each generation.

The problem comes when one compares two species of the same taxon, say two mammals, with very different generation times. Mice, for instance, go through four to five reproductive cycles a year. The number of mutations, therefore, would be dramatically higher than, say, those of an elephant.

Thus, they should not reflect similar percent sequence divergences for comparable proteins. Besides that, the rates of mutations are different for different proteins even of the same species. That means that, for the molecular clock idea to be correct, there must be not one molecular clock, but thousands.

So let me point out here that, in this section, Pandas describes the simple molecular clock idea that was proposed 40 years ago by Zuckerkandl and Pauling, and then talks about the two complications for the model, which are common knowledge and are taught in basic science texts that deal with this issue, the generation time problem and the fact that different proteins accumulate mutations at different rates.

And as I have shown from the literature I just cited, that continue to be live issues in the scientific community.

Q. In that section you read from on the molecular clock from Pandas are found on page 39, is that correct?

A. Yes, that's correct.

Q. Again, returning to that slide that Dr. Miller presented in his testimony?

A. Yes. I just wanted to go back to that slide where Dr. Miller says -- again, I should say that, in his testimony, which I attended, he, you know, excoriated Pandas on this point. And he says -- on his slide, he says, in fact, the information we have confirms that each of these organisms is equidistant from a common ancestor, which is the actual prediction of evolutionary theory.

And that's simply is incorrect. And in my view, Pandas is treating problems that Professor Miller, treating real live problems that Professor Miller shows no signs of being aware of. So I think a student reading this section would actually get a better appreciation for this subject than otherwise.

Q. Dr. Behe, in Dr. Miller's testimony, he also criticized another example found in Pandas that had a message such as, quote, John loves Mary, written on the beach, would be a sure sign of intelligence.

He claimed that any philosopher, any logician would spot the mistake in logic, because we know a human made that message, and probably made it with a stick, because we have seen such things happen in our own experience. Do you agree with this reasoning?

A. No, I disagree with Professor Miller's reasoning.

Q. And if I can just say, the example that John loves Mary, and we have a slide up, that's on page 7 of Pandas, correct?

A. Yes, that's right.

Q. Again, could you explain why you disagree with this reasoning?

A. Yes. The inference from the -- the inference from the existence of designed objects in the -- in our world of experience to the conclusion of design in life is an example of an inductive inference. And I think I explained earlier that, in an inductive inference, one always infers from examples of what we know to examples of what we don't know.

And the strength of the inference depends on similarities between the, between the inference in relevant properties. For example, in the Big Bang hypothesis, scientists extrapolated, or used inductive reasoning of their knowledge of explosions from our everyday world from things like fireworks and canon balls and so on.

They extrapolated from their experience that the motion of objects away from each other bespeaks an explosion. They extrapolated from our common everyday experience to something that nobody had ever seen before, an entirely new idea, that the universe itself began in something like a giant explosion.

Nonetheless, they were confident that this was a good idea because they thought the relevant property, the parts moving rapidly away from each other, was what we understand from an explosion. And that's how science often reasons.

In the same way, the purposeful arrangement of parts in our everyday experience bespeaks design. Pandas is exactly right, that if we saw such a message on the beach, we could conclude that it had been designed. And William Paley is exactly right, that if we stumbled across a watch in a field, that we would conclude that it was designed, because in each case there is this strong appearance of design from the purposeful arrangement of parts.

Now we have found purposeful arrangement of parts in an area where we didn't expect to, in the very cellular and molecular foundation of life, in the cell. The cell again was not understood in Darwin's day. And it is much better understood now. And from the new information we have, again, we see this purposeful arrangement of parts, and it's -- by inductive reasoning, we can apply our knowledge of what we see in our everyday world to a different, completely different realm.

And so that sort of inference has been done in science throughout the history of science, and it's a completely valid inference for Pandas to make.

Q. Now we've heard some testimony throughout the course of this trial of a program called SETI, S-E-T-I, a project, I believe, that stands for the search for extraterrestrial intelligence?

A. Yes.

Q. Are you familiar with that project?

A. Yes, I am.

Q. Whose project is that?

A. The search for extraterrestrial intelligence is a project that was, for a while, was sponsored by the federal government. It involved scientists scanning the skies with detectors to see if they could detect some electromagnetic signal that might point to intelligence.

Q. Is there a comparison with that project to the discussion you had in here with the John loves Mary on the beach?

A. Yes. Again, if they detected something that seemed to have a purposeful arrangement of parts, if they saw something that bespoke a message, then even though we have had no experience with other entities from off the Earth trying to send us a message, nonetheless, we could still be confident that an intelligent agent had designed such a message.

And again, whenever we see John -- things like John loves Mary, we can be confident of that. And when we see the purposeful arrangement of parts in the cell, the argument is that, we can be confident of that, that that bespeaks design as well.

Q. I want to bring this discussion somewhat down to the molecular level, and ask you whether or not new genetic information can be generated by Darwinian processes. And I want to be more specific and ask whether new genetic information can be generated by known processes such as gene duplication and exon shuffling?

A. Well, that's a topic about which you have to be very careful and make distinctions.

Q. Okay. Let's start with the gene duplication. If you could explain what that is in the context of generating new genetic information?

A. Well, gene duplication is a process whereby a segment of DNA gets copied twice or gets duplicated and replicated so that where one gene was present before, a second copy of the exact same gene is now present in the genome of an organism. Or sometimes larger segments can be duplicated, so you can have multiple copies of multiple genes.

Q. Are you saying, duplication, like photocopying, is just making another copy of the gene that was originally existing?

A. Yeah, that's a good point. It's important to be aware that gene duplication means that you simply have a copy of the old gene. You have not done anything new. You've just taken the same gene and copied it twice. So it would be like, like photocopying a page. And now you have two pages, but it's just a copy of the first one, it's not something fundamentally new.

It would be like saying, the example of Pandas here with John loves Mary. If you walked down the sand another five yards or something, and you came across another message that says, John loves Mary, well, that's interesting, but you don't have anything fundamentally new.

Q. Can there be variations though in the duplication of those genes?

A. Well, once a gene has duplicated, then the idea goes that, perhaps one of those two copies can continue to perform the function that the single copy gene performed before the duplication, and the other one is sort of a spare copy.

Now it's available to perhaps undergo mutation, and mutation accumulate changes, and perhaps Darwinian theory postulates. Perhaps it can go on to develop brand new properties.

Q. Does this generate new information? And if you use that John loves Mary example to help explain perhaps?

A. Well, again, you have to be careful. Nobody disputes that random mutation and natural selection can do some things, can make some small changes in pre-existing systems. The dispute is over whether that explains large complex functional systems.

And to leave the world of proteins for a second, to look at John loves Mary, suppose we're looking at the spare copy, and the first copy was continuing to fulfill the function of conveying that information. Well, you know, suppose you changed a letter. Suppose you changed the final n in the word John to some other, some other letter, like r. That would not spell a name in the English language.

So that's kind of an analogy to saying that, you might lose the function of the message in the terms. In the terms of protein, the protein might no longer be functional. But you might get to closeby. You might get to closeby messages. For example, if you deleted the r and the y from the end of Mary, you might get to John loves Ma, or some such thing. But you're not going to get anything radically different from that.

Q. So you are operating with the copy. The copy is operating with those same letters, the John loves Mary, or some variation or deletions of that subset?

A. That's right. A copy is a copy. It's essentially the same thing. And now the big problem that Darwinian processes face is, now what do you do? How do you generate a new complex function?

Q. And that's with gene duplication that we just talked about. Could you explain a little bit about exon shuffling in the context of generating new complex information?

A. Yes, exon shuffling is a little bit more involved. It turns out that the gene for a protein can contain regions of DNA that actually code for regions of a protein interrupted by regions of DNA that don't code for regions of a protein. And the regions that code for the part of the protein are called exons.

Now it turns out that, in cellular processes, similar to gene duplication and other processes, too, one can duplicate separate exons and sometimes transfer them to different places in the genome and other such processes. But to make it more understandable, we can go back to the analogy of John loves Mary.

And in this sense, exon shuffling might be expected to generate something like, instead of John loves Mary, perhaps Mary loves John, or John Mary loves, or something like that. But again, it's kind of a mixture of pre-existing properties, and we're not generatesing something fundamentally new.

Q. So, for example, you couldn't generate Brad loves Jen from exon shuffling using your beach example?

A. No, I hope not.

Q. Do these concepts, particularly gene duplication, exon shuffling, do they have any impact on the concept of irreducible complexity that you've been discussing quite a bit throughout your testimony?

A. Yes. In fact, there is an important point to recognize here. Russell Doolittle knew all about the processes of gene duplication and exon shuffling. And as a matter of fact, in the blood clotting cascade, many proteins look similar to each other, and they're often times pointed to as examples of exon shuffling.

But nonetheless, that knowledge did not allow him to explain how the blood clotting system might have arisen. Again, these are sequence comparisons. And such information simply does not speak to the question of random mutation and natural selection being able to build complex new biochemical structures.

In the same way, the people who are investigating the type III secretory system and the bacterial flagellum know all about gene duplication and exon shuffling. And nonetheless, that information has not allowed them to explain the origin of either of those structures.

So those are interesting processes. And people who are convinced of Darwinian theory include those processes in their theory, but they do not explain -- they do not explain where new complex systems come from. And it's an example of somebody accommodating this information to an existing theory rather than getting information that actually experimentally supports the theory.

Q. So can random mutation and natural selection generate new information?

A. Well, again, that's -- you have to be careful. You can make small changes in pre-existing systems. And that's clearly the case. One can clearly do that. But there has been no demonstration to show that such processes can give rise to new complex systems such as we've been suggesting. And there are many reasons to think that it would be extremely difficult to do so.

Q. Have you prepared some slides with a couple -- several quotes that make this point?

A. Yes, I do. This first one is an excerpt from a paper from John Maynard Smith, which I spoke about earlier, from 1970 entitled Natural Selection and the Concept of a Protein Space. Let me read the first excerpt.

Quote, It follows that if evolution by natural selection is to occur, functional proteins must form a continuous network which can be traversed by unit mutational steps without passing through nonfunctional intermediates, close quote. Again, let me explain.

If you can remember the figure of two proteins binding to each other that I showed in -- I showed yesterday, he is speaking of unit mutational steps in terms of one of those interactions, maybe a plus charge and a minus charge or a hydrophobic group and another hydrophobic group.

And so to get two proteins to -- or proteins to start change into something new and different with different properties, each one of those changes would have to be a beneficial one, or at least not cause any difficulties for the problem. And actually, seeing how that could happen is extremely difficult.

And continuing on this slide. I'm sorry. Could you back up one slide? Thank you. The bottom part of the quotation, he says, quote, An increase in the number of different genes in a single organism presumably occurs by the duplication of an already existing gene followed by divergency. So here, he's kind of describing the standard scenario which -- scenario, which is standard in Darwinian thinking, that one has gene duplication and then divergence of the sequence of a gene, and that gives a brand new interesting and complex protein.

But notice that I, of course, underlined and bolded the word presumably. Well, presumably, you know, is a presumption. And it may be true, and it may not. But presumptions are not evidence. And so in order to support this idea, one needs more than the presumption that it occurs.

Q. Do you have another citation to a science text?

A. Yes, I do. Here's an excerpt from an article by a man named Alan Orr, who is an evolutionary biologist at the University of Rochester. And again, this speaks to the same consideration, that you have to be able to have a pathway that step by tiny step could lead from one functional protein to another.

He says, quote, Given realistically low mutation rates, double mutants will be so rare that adaptation is essentially constrained to surveying, and substituting, one mutational step neighbors. Thus, if a double mutant sequence is favorable, but all single amino acid mutants are deleterious, adaptation will generally not proceed.

Again, this makes the point that, if you only need to change one little step, Darwinian evolution works fine. But if you need to change two things before you get to an improved function, the probability of Darwinian processes drops off dramatically.

If you need three things, it drops off, you know, even more dramatically. And nonetheless, as I showed in that figure of interacting proteins, even to get two proteins to stick together, multiple groups are involved.

Q. Did you write about something similar in a paper?

A. Yes. The paper that I published with David Snoke last year speaks exactly to this topic. It's entitled Simulating Evidence by Gene Duplication of Protein Features that Require Multiple Amino Acid Residues.

And in this theoretical study, we showed that, again, if you need one change, that's certainly doable. If you need two amino acid changes before you get a selectable function, the likelihood of that drops considerably. Three or more, now you're really in the very, very improbably range. So again, gene duplication is not the answer that it's often touted to be.

Q. Can you make an analogy here at all to -- you talked about Maxwell and the ether theory?

A. Yes. When Darwinian -- adherence to Darwinian theory, when they view that there are similar genes in different -- in the same organism, and they infer a process of gene duplication, it is simply their theoretical framework, which is saying, such a process must be important in generating new and complex structures.

That has not been demonstrated. Just like James Clerk Maxwell knew that light was a wave and inferred from his theory that there must be an ether, modern Darwinists infer from something we know, the existence of gene copies to an unproved role of such a process in generating complex biochemical systems.

Q. Now Dr. Miller says that Pandas necessarily rejects common descent, and points to a figure -- I believe it was 4.4 on page 99 -- showing separate lines representing categories of animals rather than a branching tree. Do you regard that as ruling out common descent?

A. No, I don't. And here's a figure that I made up in the upper right-hand corner. It's figure 4.4 from Pandas, which is the figure that Professor Miller showed, which shows straight lines instead of a branching tree, which is the traditional representation of how -- of the fossil record.

Nonetheless, here I regard this as simply trying to describe the data without a theoretical framework, without the branched lines in between. One has to realize that these lines do not occur in the fossil record. These are theoretical constructs.

And how one groups things together is theory building rather than data itself. I viewed this as Pandas trying to describe the data without the framework of the existing theory. And I might add that, this was figure 4.4. And earlier, a couple pages earlier, Pandas describes the traditional interpretation of the fossil record in terms of a branching tree.

And in this section, section 96 through 100, the meaning of gaps in the fossil record, Pandas describes the traditional tree diagram for the fossil record, and then points to statements by biologists, saying that there seem to be difficulties in this sort of representation, and then goes on to discuss what interpretations, what ideas have been offered to try to account for the form of the fossil record.

Pandas writes, Several interpretations have been offered to resolve this problem. That is, that the tree of life doesn't seem to be as continuous as one might expect. Number 1, they say, imperfect record. That is, maybe not all organisms left representative of fossilized specimens. Number 2, incomplete search. And that is, maybe we simply haven't looked in the right places or looked in all the places on the Earth, and maybe when we do, then we will find what we expect to be there.

Number 3, what they call jerky process, or which has been called punctuated equilibrium, which was an idea advanced by Steven J. Gould and Niles Eldredge in the 1970's, whereby it said that the mode or the tempo of evolution is one in which a species or a branch of life stays pretty much constant for a long period of time, and then within a relatively short period of time, large changes occur.

And then fourth, they say, well, perhaps -- they suggest something called the sudden appearance or face value interpretation, saying that, well, maybe if we see the sudden appearance of some feature or organism in the fossil record, then that, in fact, might be what happened.

Nonetheless, as I say, they discuss all of these possibilities, including the standard interpretation. And at the end of the section, they write that, scientists should not accept the face value interpretation of the fossil record without also exploring the other possibilities, and even then, only if the evidence continues to support it.

So as I read this, Pandas is telling students that they should follow the data where the data lead. And if the data lead from this model to another model, or from that model to a second model, then a scientific attitude toward the problem is to follow the data, where the data go.

Q. Dr. Behe, does intelligent design necessarily rule out common descent?

A. No, it certainly does not.

Q. Now we've heard testimony from several witnesses claiming that the theory of evolution is no different than, say, the germ theory of disease, so there's no reason to pay any special attention to it. Do you agree with that?

A. No, I disagree.

Q. And why?

A. Well, in a number of ways, evolutionary theory is unique. It's been my experience that students have a number of misconceptions about the theory. They confuse facts with theoretical interpretations. They do not make distinctions between the components of evolutionary theory.

And perhaps, most strikingly, a number of people have made very strong extra-scientific claims for the implications of evolutionary theory.

Q. Now I just want to return to something you had said about your experience with students. You testified that you teach a course called popular arguments on evolution, is that correct?

A. Yes, that's right.

Q. And you've been teaching that for 12 years?

A. Roughly, yes.

Q. Now are there some standard misconceptions that you can point to about the theory of evolution that you find your students bringing to the class?

A. Yes. In my experience, a number of students come in thinking that, in fact, evolution is completely true; that is, they don't make a distinction between fact and theory, they don't think it will be falsified, or they don't think there's a possibility of it being falsified.

They also confuse various components of evolutionary theory. For example, you can ask a student, you know, why they think Darwinian evolution is correct? And they'll say, you know, because, you know, because of the dinosaurs. And they're mistaking change over time with the question of natural selection. And they will assume that the existence of animals in the past necessarily means that animals in the present were derived from them by random mutation and natural selection.

Oftentimes also, students think that utterly unsolved problems, such as the origin of life, have, in fact, been solved by science. I had students tell me that, gee, it's true, right, that science has shown genes being produced in origin of life experiments. So in my experience, students bring a number of misconceptions to this issue.

Q. One of the first ones you indicated is that they believe that Darwin's theory of evolution is a fact as opposed to a scientific theory?

A. That's right.

Q. Does intelligent design seek to address some of these misconceptions?

A. Yes. Yes, it does. One way is -- one way to address the problem of students not understanding that the distinction between fact and theory is to at least have at least one more theoretical framework in which to treat facts.

If a student has only one theory and a group of facts to think of, it's extremely difficult to distinguish what is theory and what is fact. The little lines connecting various points on, say, a protein sequence comparison are theory, but students can often confuse them, confuse them to be facts.

Q. Do you believe these students will be better prepared if they had learned that Darwin's theory of evolution was not a fact and that gaps and problems existed within this theory?

A. Yes, I certainly do. They would see that, in fact, if you can look at the data in a couple ways, then they'll more easily distinguish data from interpretation or from theory. And if they are aware that there are problems in a theory, then perhaps they won't expect -- they won't, again, confuse it with a fact, they'll understand that there are some problems that are unresolved.

Q. Now you made some indication previously in your answer to my question that there are claims made about the theory that go beyond biology, is that true?

A. Yes, that's certainly true.

Q. And do you have some slides to demonstrate some of those examples?

A. Yes, I have a couple of slides, four slides over -- that point to this. For example, in the high school textbook Biology, which was written by Professor Kenneth Miller and his co-author, Joseph Levine, this is the 1995 version, I think, the third edition, in a section entitled The Significance of Evolutionary Theory, the authors write, quote, The influence of evolutionary thought extends far beyond biology. Philosopher J. Collins has written that, quote, there are no living sciences, human attitudes, or institutional powers that remain unaffected by the ideas released by Darwin's work, close quote.

In another example of the implications, the profound implications beyond biology that some people see for Darwin's theory, there's a section in his book, Finding Darwin's God, A Scientist's Search for Common Ground Between God and Evolution, where Dr. Miller writes that, quote, God made the world today contingent upon the events of the past. He made our choices matter, our actions genuine, our lives important. In the final analysis, He used evolution as the tool to set us free.

So here is a scientific theory which is being used to support the idea that we are free, we are free, in apparently some metaphysical sense, because of the work of Darwin. In another example -- it's just that -- for example, the expert, Professor John Hauck, the theologian from Georgetown University, has written a number of books, including God After Darwin, a Theology of Evolution.

Further example, in -- the evolutionary biologist, Richard Dawkins, in his book, The Blind Watchmaker, writes, Darwin made it possible to be an intellectually-fulfilled atheist.

If I could have the next slide. Thank you. The Darwinian philosopher, Daniel Dennett, who's at Tufts University, has described Darwinism as a universal acid that destroys our most cherished beliefs. And he says, quote, Darwin's idea had been born as an answer to questions in biology, but it threatened to leak out, offering answers, welcome or not, to questions in cosmology, going in one direction, and psychology, going in the other direction.

If the cause of design in biology could be a mindless, algorithmic process of evolution, why couldn't that whole process itself be the whole product of evolution, and so forth, all the way down? And if mindless evolution could account for the breathtakingly clever artifacts of the biosphere, how could the products of our own real, quote, unquote, minds be exempt from an evolutionary explanation? Darwin's idea thus also threatened to spread all the way up, dissolving the illusion of our own authorship, our own divine spark of creativity and understanding.

So again, Professor Dennett sees implications for Darwin's theory that are profound and that extend well beyond biology. Another philosopher by the name of Alex Rosenberg, who's at Duke University, published an article a few years ago in the journal Biology and Philosophy that, quote, No one has expressed the destructive power of Darwinian theory more effectively than Daniel Dennett. Others have recognized that the theory of evolution offers us a universal acid, but Dennett, bless his heart, coined the term.

In short, it, that is Darwin's idea, has made Darwinians into metaphysical Nihilists denying that there is any meaning or purpose to the universe, close quote. So again, a number of philosophers, a number of scientists, and so on, see very, very profound implications in Darwin's theory.

Two more quotations on this last slide on this topic. Larry Arnhart is a professor of political science at Northern Illinois University. He wrote a book entitled Darwinian Natural Right, The Biological Ethics of Human Nature. And in it, he writes -- and in it, he writes the following, that, quote, Darwinian biology sustains conservative social thought by showing how the human capacity for spontaneous order arises from social instincts and a moral sense shaped by natural selection in human evolutionary history.

So let me emphasize that he sees implications for politics from Darwin's theory. And the same -- and a Princeton University philosopher by the name of Peter Singer has written a book entitled A Darwinian Left, Politics, Evolution, and Cooperation. And in it, he writes that we should try to incorporate a Darwinian ethic of cooperation into our political thought.

So the gist of Professor Singer's book is that, Darwinian ideas support a liberal political outlook. And he argues for that. So, again, these -- all of these people see profound implications for Darwin's theory well far beyond biology.

Q. These are non-scientific claims, correct?

A. Yes, that's correct.

Q. Have you come across any similar claims made about, say, the germ theory of disease?

A. I have never seen the germ theory of disease argued to say how we should conduct our political life.

Q. How about atomic theory?

A. I have never seen atomic theory used in such profound senses either. So my point then is that, it is perfectly rationale to treat a scientific theory, which so many people have claimed such profound implications for, to treat it differently from other scientific theories for which such far-reaching implications have not been claimed.

It might be very important, and I think a school district would be very justified to say that, since this particular theory seems to reach far beyond its providence, then we should take particular care in explaining to our students exactly what the data is for this theory, exactly what is the difference between theory and fact, exactly what is the difference between theory and interpretation. And so I think such an action would be justified.

Q. Sir, I want to ask you some questions about creationism as it relates to intelligent design. First of all, let me ask you, does creationism have a popular meaning or is there a popular understanding of that term?

A. Well, again, you have to be careful, because many words in these discussions can have multiple meanings. And if you're not very careful about your definitions, you'll easily become confused.

Creationism -- creationist has sometimes been used, as John Maddox, the editor of Nature, used it, simply to mean somebody who thinks that nature was begun by a supernatural act, by God, and the laws of nature perhaps were made of God, and unfolded from there nonetheless.

Q. That would be similar to Dr. Miller's view towards evolution that he had written in his book Finding Darwin's God?

A. Yes, that seems to be consistent with what he wrote. But nonetheless, in the popular useage, creationism means -- creationist means somebody who adheres to the literal interpretation of the first several books -- or first several chapters of the Book of Genesis in the Bible, somebody who thinks that the Earth is relatively young, on the order of, say, 10,000 years, that the major groups of plants and animals and organisms were created ex-nihilo in a supernatural acts by a supernatural being, God, that there was a large worldwide flood which is responsible for major features of geology, and so on.

Q. Now we've heard different terms; young-earth creationism, old-earth creationism, and special creationism. And you have familiarity with those terms, is that correct?

A. Yes, that's right.

Q. Is intelligent design creationism, whether you call it young-earth creationism, old-earth creationism, or special creationism?

A. No, it is not.

Q. And why not?

A. Creation -- creationism is a theological concept, but intelligent design is a scientific theory which relies exclusively on the observable, physical, empirical evidence of nature plus logical inferences. It is a scientific idea.

Q. Is it special creationism?

A. No, it is not special creationism.

Q. Again, why not?

A. Again, for the same reason. Creation is a theological religious concept. And intelligent design is a scientific idea, which is based exclusively on the physical, observable evidence plus logical processes.

Q. Dr. Miller has made a claim that if the bacterial flagellum, for example, was designed, then it had to be created, and is, therefore, special creationism. Is that accurate?

A. No, that is inaccurate. The reason it's -- again, creation is a theological concept. It is a religious concept. But intelligent design is a completely scientific concept which supports itself by pointing to observable, physical, empirical facts about the world, about life, and makes logical inferences from them.

Q. Does intelligent design require that the bacterial flagellum, for example, instantaneously appear from nothing?

A. No, it does not.

Q. Why not?

A. Because intelligent design focuses exclusively on the deduction of design from the purposeful arrangement of parts. And it says nothing directly about how the design was effected, whether it was done quickly, or slowly, or whatever. So it has nothing to say about that.

Q. Could the bacterial flagellum have been designed over time?

A. Yes, it could.

Q. Does intelligent design require ex-nihilo creation?

A. No, it does not.

Q. Why not?

A. Because again, the term ex-nihilo creation is a theological concept, a religious concept. And intelligent design is a scientific idea that relies on observable facts about nature plus logical inferences.

Q. Is there, again, an analogy you can make here to the Big Bang theory?

A. Yes. Yes, there is. Again, many people, including many scientists, saw in the Big Bang theory something that had theological implications, maybe this, this Big Bang was ex-nihilo creation by a supernatural being. And many people who saw that didn't like that. Nonetheless, the Big Bang theory itself is an utterly scientific theory because it relies on observations, physical observations, empirical observations about nature, and reasons from those observations using logical processes.

Q. Is intelligent design a religious belief?

A. No, it isn't.

Q. Why not?

A. Intelligent design requires no tenet of any particular religion, no tenet of any general religion. It does not rely on religious texts. It does not rely on messages from religious leaders or any such thing. The exclusive concern of intelligent design is to examine the empirical and observable data of nature and reason from that using logical processes.

Q. Now some claim that intelligent design advances a religious belief, that it is inherently religious and not science. Do you agree?

A. No. Again, no more than the Big Bang theory is inherently religious. Although the Big Bang theory and intelligent design might be taken by some people to have theological or philosophical implications, both of them rely on observed evidence, empirical evidence, and logical reasoning.

Neither the Big Bang nor intelligent design relies on any religious tenet, points to any religious books, or any such thing.

Q. Do creationists in the sense that Plaintiffs and, I believe, their experts use in this case require physical evidence to draw their conclusions?

A. No. Actually, it's interesting that one could be a creationist without any physical evidence. One could rely -- a creationist could rely for his belief in creation on, say, some religious text or in some private religious revelation or some other non-scientific source.

So a creationist does not need any physical evidence of the kind that, for example, Richard Dawkins sees in life that leads him to think that life has the strong appearance of design or the kind that David DeRosier sees in the bacterial flagellum. A creationist can believe in creation without any such physical evidence.

Q. Is that different than from a proponent of intelligent design?

A. Yes, that's vastly 180 degrees different from intelligent design. Intelligent design focuses exclusively on the physical evidence. It relies totally on empirical observations about nature. It does not rely on any religious text. It does not rely on any other such religious information. It relies exclusively on physical evidence about nature and logical inferences.

Q. Are intelligent design's conclusions or explanations based on any religious, theological, or philosophical commitment?

A. No, they are not.

Q. Again, can you draw any comparisons between intelligent design and the Big Bang theory in this regard?

A. Yes. Again, the -- both the Big Bang theory and intelligent design may have philosophical or theological implications in the view of some people, but again, both are scientific theories. Both rely on observations about nature. Both make reasoned conclusions from those observations about nature.

Q. Does intelligent design require adherence to the literal reading of the Book of Genesis?

A. No, it does not.

Q. Does intelligent design require adherence to the belief that the Earth is no more than 6 to 10,000 years old?

A. No, it doesn't.

Q. Does intelligent design require adherence to the flood geology point of view which is advanced by creationists?

A. No, it doesn't.

Q. Does intelligent design require the action of a supernatural creator acting outside of the laws of nature?

A. No, it doesn't.

Q. Could you explain?

A. Yes. Making an analogy again to the Big Bang theory, the Big Bang theory is a theory which is advanced simply to explain the observations that we have of nature, and it does so by making observations and making inferences. It does not posit any supernatural act to explain the Big Bang. It leaves that event unexplained.

Perhaps in the future, science will find an explanation for that event. Perhaps it won't. But nonetheless, the Big Bang is a completely scientific theory. Again, intelligent design is a scientific theory that starts from the data -- the physical, observable data of nature, and makes reasoned conclusions from that and concludes intelligent design.

Scientific information does not say what is the cause of design. It may never say what is the cause of design. But nonetheless, it remains the best scientific explanation for the data that we have.

Q. Can science then identify the source of design at this point?

A. No, not at this point.

Q. Does intelligent design rule out a natural explanation for the design found in nature?

A. No, it does not rule it out.

Q. Could you explain?

A. Yes. Again, harkening back to the Big Bang theory, the Big Bang theory was proposed, and the cause of the Big Bang was utterly unknown. It's still utterly unknown. But nonetheless, the Big Bang theory is a scientific theory.

The Big Bang theory does not postulate that the Big Bang was a supernatural act. Although, you know, it simply posits no explanation whatsoever. In the same sense, intelligent design is a scientific theory advanced to offer -- advanced to explain the physical, observable facts about nature.

It cannot explain the source of the design and just leaves it as an open question.

Q. We've heard testimony about methodological naturalism. Are you familiar with that term?

A. Yes, I am.

Q. I believe you indicated in your deposition that you thought it hobbles or even constrains intelligent design, is that correct?

A. Yes, that's right.

Q. How does it do so?

A. Well, any constraint on what conclusion science can come to hobbles all of science. Science should be an open, no-holds-barred struggle to obtain the truth about nature. When you start putting constraints on science, science suffers.

Yesterday, I discussed a man named Walter Nernst who said that the timelessness of nature, the infinity of time was a necessary constraint on a scientific theory. Science had to operate within that framework. If he had prevailed, progress, real progress in science would have been severely constrained.

Another reason why methodological naturalism can be a constraint on science is because oftentimes people don't think -- don't separate neatly categories in their own minds. For example, I showed the -- I showed the quotation from John Maddox, the editor of Nature, who found the Big Bang theory philosophically unacceptable and was reluctant to embrace it because of that.

There are other scientists in the past, one named Fred Hoyle, who rejected the Big Bang theory because he did not like its non-scientific, extra-scientific implications. So to the extent that people confuse a scientific theory with extra-scientific implications that some people might draw from it, then that might -- that might be a constraint upon the theory.

Q. Despite these constraints, does intelligent design still fit within the framework of methodological naturalism?

A. Yes. Despite the constraints, it certainly does, just as the Big Bang theory does.

Q. Now we've heard some testimony about space aliens and time traveling biologists. And I believe you made some similar reference to that in your book, Darwin's Black Box, is that correct?

A. Yes.

Q. And why was that?

A. Well, this was, you know, a tongue-in-cheek effort to show people that, you know, intelligent design does not exclude natural explanations, although some, you know, explanations we might wave our hands to think up right now might strike many people as implausible, they are not, you know, utterly illogical.

And it was kind of a placemaker to say that maybe some explanation will occur to us or be found in the future which will, in fact, be a completely natural one.

Q. Now the space alien claim in particular seems to fall hard on the ear of a lay person. But has that been a claim that has been advanced by a notable scientist to explain the natural phenomena?

A. Yes, that's right. Surprisingly, in the year 1973, a man named Francis Crick, the eminent Nobel laureate who discovered the double helicle shape of DNA with James Watson, he published, with a co-author named Leslie Orgle, he published a paper entitled Directed Panspermia, which appeared in the science journal Icarus.

And the gist of the paper was that the problems trying to think of an unintelligent origin of life on Earth were so severe that perhaps we should consider the possibility that space aliens in the distant past sent a rocket ship to the Earth filled with spores to seed life on the early Earth.

Q. This was a claim advanced by a Nobel laureate?

A. Yes, Francis Crick.

Q. And the article in which his arguments appear, was this a peer reviewed science journal?

A. Yes, the journal Icarus.

Q. Was this just a tongue-in-cheek, so to speak, explanation on behalf of Francis Crick?

A. No, it wasn't. He mentioned it first in that 1973 article, and he repeated the same claim in a book he published in '88 and interviews he gave later on. And from what I understand, he still thought it was a reasonable idea up until his death recently.

Q. Sir, I'd ask you to direct your attention to the exhibit binder that I have provided for you, and if you could go to tab 14. There is an exhibit marked as Defendants' Exhibit 203-E as echo. Is that the article from Francis Crick that you've been testifying about?

A. Yes, this is Francis Crick's article on Directed Panspermia.

Q. Is the search for intelligence causes a scientific exploration?

A. Yes, it is.

Q. Again, do you have any examples that we could point to?

A. Well, one good example is one that I mentioned earlier, which is this project called the SETI project, S-E-T-I, which stands for search for extraterrestrial intelligence, where scientists use instruments to scan space in the hope of finding transmissions or some signals that may have been sent by extraterrestrial sources.

And they are confident that they could be able to distinguish those signals from the background noise, background radiation, electromagnetic phenomena of space.

Q. Again, that's a scientific exploration?

A. Yes, a number of scientists are involved in that.

MR. MUISE: Your Honor, I'm just -- do you intend to go to 12:30?

THE COURT: I was thinking more 12:15, unless you think that this is an appropriate break point. Your call.

MR. MUISE: I certainly have more than 15 minutes. This next section might be divided in that 15, so my preference would be to take the lunch break and come back and then complete the direct during the first session after lunch.

THE COURT: All right. We'll return then at, let's say, 1:25, this afternoon, after a suitable lunch break, and we'll pick up with your next topic on direct at that time. We'll be in recess.

(Whereupon, a lunch recess was taken at 12:04 p.m.)

(1:25 p.m., convene.)

(Direct examination of Dr. Michael J. Behe continued.)

THE COURT: Be seated, please.

A.ll right, back to you, Mr. Muise.

MR. MUISE: Thank you, Your Honor. May I approach the witness?

THE COURT: You may.

BY MR. MUISE:

Q. Dr. Behe, I've handed you what's been marked as defendant's exhibit 220, which is a copy Of Pandas and People, the second edition. Do you see that?

A. Yes, I do.

Q. I would like to direct your attention to page 99, please. I would like to read to you and oft-quoted passage in this case thus far. If you'll look at the bottom on page 99, it's going to continue onto 100 as well. It says, quote, Intelligent design means that various forms of life began abruptly through an intelligent agency with their distinctive features already intact: Fish with fins and scales, birds with feathers, beaks and wings, et cetera. Some scientists have arrived at this view since fossil forms first appeared in the record with their distinctive features intact and apparently fully functional rather than gradual development.

And I would like to get your reaction to that section?

A. Well, it says -- it says that some scientists have arrived at this view. I think that's a way of saying that this is a matter of disagreement and dispute.

I certainly do not think that intelligent design means that a feature has to appear abruptly. And I -- I certainly would have written this differently if I had done so.

Q. Now, you say you would have written it differently. Is there another reference or another section in Pandas that you could direct us to to emphasize that point?

A. Yes. I wrote the section at the end of Pandas which is discussing blood clotting. And on page 144 of the text there's a section entitled "A Characteristic of Intelligent Design." And it begins, "Why is the blood clotting system an example of intelligent design? The ordering of independent pieces into a coherent whole to accomplish a purpose which is beyond any single component of the system is characteristic of intelligence."

Q. And why did you direct us to that particular section?

A. Because I think it more clearly conveys the central idea of intelligent design, which is the purposeful arrangement of parts.

Q. Do you see that then as a, perhaps a better characterization, or more accurate characterization of intelligent design?

A. Yes, I like this a lot better.

Q. Now I want to read you a couple of quotes regarding this notion of abrupt, or abrupt appearance. This one is from Ernst Mayr, from One Long Argument, which is one of the documents you had referenced in your testimony. It says, quote, Paleontologists have long been aware of a seeming contradiction between Darwin's partial of gradualism and the actual findings of paleontology. Following phyletic lines through time seem to reveal only minimal gradual changes but no clear evidence for any change of a species into a different genus or for the gradual origin of an evolutionary novelty. Anything truly novel always seem to appear quite abruptly in the fossil record, end quote.

I want to read you one more quote, and this is from a writing by a gentleman whose last name is Valentine. Quote, It is this relatively abrupt appearance of living phyla that have been dubbed the Cambrian Explosion, end quote.

Do you see those -- those references to abrupt that I just read to you comparable to the reference in Pandas?

A. Yes, they seem to be talking about the same things.

Q. Well, Dr. Padian, if my recollection is correct, testified that the two were speaking of different things, the quotes that I read to you were speaking of abrupt in the sense of geological time whereas Pandas is not speaking so much to that effect.

MR ROTHSCHILD: Objection, it's mischaracterizing Dr. Padian's testimony.

THE COURT: In what sense?

MR ROTHSCHILD: Dr. Padian is referring to the appearance of fossils in the record, not to the abrupt appearances of creatures for the first time. He's not talking about, in the sense of geological, he's talking about the fossils -- when we find fossils.

THE COURT: Well, the precursor to your question assumed that you weren't sure if you had it right. If you're going to cite to Dr. Padian's testimony, you ought to be sure.

MR. MUISE: Your Honor, I can ask a question, I think, which I think I have a pretty decent recollection of what it was. But I can ask the question where I don't have to refer to Dr. Padian but I think it will achieve the objective.

THE COURT: That might resolve the problem. If you're going to try to paraphrase Dr. Padian without referring to a transcript I think you're going to get potentially some difficulty. So I'll sustain the objection on that basis. You can rephrase.

BY MR. MUISE:

Q. Dr. Behe, do you see -- well, those quotes that I -- that I read to you, and the quote out of Pandas which you read, you already testified that you see them similar in a sense. Do you see that they're similar in a sense that abrupt is speaking to this -- a concept in geological time?

A. Yes. Pandas is speaking of the fossil record, from what I read. So how else can we tell about the appearance except the appearance in the fossil record? So I think it's -- it's exactly the same. It's the appearance, the abrupt appearance, as Mayr and James Valentine said, of these things in the fossil record.

Q. You indicated that intelligent design doesn't require abrupt appearance, is that correct?

A. Yes, that's right.

Q. Does it say anything directly about the pace of change?

A. No. Again, intelligent design simply is the theory that designed features can be detected from the physical -- physical evidence of nature, it's seen in the purposeful arrangement of parts, but it does not say anything directly about how fast such a thing might go, how slow such a thing might go, or other interesting questions.

Q. And if there's an abrupt appearance of fossils in the record, would that be consistent or inconsistent with intelligent design?

A. It's completely consistent with intelligent design. An abrupt appearance, a slow appearance; intelligent design does not speak to the pace of such things.

Q. And I believe you testified previously you would have perhaps written that section differently.

A. Yes. The way I would have put it is the way I did put it in the section on blood clotting.

Q. I d like to ask you to turn to page 100 of Pandas. I want to continue down on that same section.

And it says, quote, This alternative suggests that a reasonable, natural cause explanation for origins may never be found, and then intelligent design best fits the data, end quote.

And I d like to get your reaction to that sentence.

A. Well, it seems perfectly sensible to me. It seems quite correct. We currently don't have a natural cause explanation. We might never have one. But a natural cause explanation is not being ruled out. And the development of a natural cause explanation in the future is not being ruled out. And you know it s, again, it's likened to the Big Bang theory.

The Big Bang theory did not postulate a natural cause explanation for the Big Bang. We don't currently have a natural cause explanation for the Big Bang. We may never have a natural cause explanation for the Big Bang. But nonetheless, the Big Bang theory is thought by physicists to best fit the data that we currently have. And right now I think intelligent design also best fits data that we currently have.

Q. So Dr. Behe, do you think Pandas would be a good book, a good reference book for students to have access to?

A. Yes, I do.

Q. And why is that?

A. Well, because in order to best discern the difference between facts and theories, it's extremely useful to be able to view facts from a couple of different theoretical perspectives. It would help a student separate theory from facts. It would help show a student that the strength of facts, the strength of support that facts lend to a theory can oftentimes depend on a theory -- excuse me, a theoretical perspective somebody committed to a theory might see the facts as more strongly fitting the theory than somebody else. It also might help the student see that difficulties with the theory -- the strengths of the difficulties are also relative to the viewpoints that people bring to the table, that somebody who views a theory as very strongly supported already like, for example, the ether theory of light, will view difficulties with the theory a lot differently and perhaps a lot more permissively than somebody who does not share the same theoretical perspective. So I think it would be very good for that purpose.

Q. So you're aware that a statement is read to students at Dover High School?

A. Yes.

Q. And I would like to read to you the statement, and I'll represent to you this is the statement that was prepared to be read in January of 2005: "The Pennsylvania academic standards requires students to learn about Darwin's theory of evolution, and eventually take a standardized test of which evolution is a part. Because Darwin's theory is a theory, it continues to be tested as new evidence is discovered. Theory is not a fact. Gaps in the theory exist for which there is no evidence. A theory is defined as a well-tested explanation that unifies a broad range of observations. Intelligent design is an explanation of the origin of life that differs from Darwin's view. The reference book Of Pandas and People is available for students who might be interested in gaining an understanding of what intelligent design actually involves. With respect to any theory, students are encouraged to keep an open mind. The school leaves the discussion of the origins of life to individual students and their families. As a standards-driven district, class instruction focuses upon preparing students to achieve proficiency on standard-based assessments."

Is it your understanding that's the statement that is read to the students?

A. Yes.

Q. Did I say anything in that short statement that in your expert opinion would cause any harm to a student's science education?

A. No, I can't see anything.

Q. Now, the first paragraph says, "The Pennsylvania academic standards requires students to learn about Darwin's theory of evolution and eventually take a standardized test of which evolution is a part."

What does that say to you?

A. If I were a student it would say that I was going to be tested on evolution, so if I wanted to do well that I should study hard.

Q. The second paragraph, "Because Darwin's theory is a theory, it continues to be tested as new evidence is discovered. Theory is not a fact. Gaps in the theory exist for which there is no evidence. A theory is defined as a well-tested explanation that unifies a broad range of observations."

Is that accurate?

A. Yes, all those sentences sound exactly accurate, and the students should understand those.

Q. "Intelligent design is an explanation of the origin of life that differs from Darwin's view. The reference book Of Pandas and People is available for students who might be interested in gaining an understanding of what intelligent design actually involves."

Do you have any problem with that paragraph?

A. That sounds like -- sounds fine as well.

Q. And finally, "With respect to any theory, students are encouraged to keep an open mind. The school leaves the discussion of the origins of life to individual students and their families. As a standards-driven district, class instruction focuses upon preparing students to achieve proficiency on standard-based assessments."

What does that say to you?

A. That sounds reasonable as well.

Q. And do you think it's good advice to inform students that with respect to any theory they ought to be encouraged to keep an open mind?

A. I think it's very good advice to pass on.

Q. Now, Dr. Alters, who testified in this case, reviewing that same one-minute statement that I read to you, said this: Quote, Now, what this policy is doing is saying there is this other scientific view that belongs, it belongs in the game of science, and it's the one that most students will perceive as God friendly. It has as intelligent designer; evolution doesn t. Now, students are going to be in there discussing out in the playground, discussing in their class, among themselves, or whatever, that the unit that they're now about to hear about, the evolution unit that's now coming up, is the one that's not God friendly, the one scientific theory that doesn't mention God; but this other so-called scientific theory, intelligent design, is God friendly, because there's a possibility that God has this other theory. What a terrible thing to do to kids. I mean, to make them have to think about defending their religion before learning a scientific concept. How ridiculous. This is probably the worst thing I ever heard of in science education."

What is your reaction to that opinion?

A. It's strikes me as, what shall I say, histrionic even. It seems utterly unconnected to the text of the statement that you just read a minute ago.

I can't see any connection between what Dr. Alters said and the statement that you read. You know, it makes me suspect that the reaction has more to do with Dr. Alters conceptions and misunderstandings and other things than it has to do with the statement itself.

Q. Dr. Padian offered his opinion that this one-minute statement would cause confusion for students and have them wondering such things as what good is prayer and why is there suffering.

What is your reaction to those claims?

A. It's hard to -- it's hard to know what to say to something like that. A couple things is -- again, you know, it strikes me as utterly unconnected to the text of the statement that was read, and I can't imagine where Professor Padian is getting this from.

I doubt that it's from his paleontological expertise. And, again, it makes me think that -- that it says more about where he's coming from, more about where -- what he's thinking, his frame of mind, than it says about the statement itself.

Q. Sir, you're aware that a newsletter was sent out by the district that discussed some of the biology curriculum?

A. Yes.

Q. I want to ask you some section -- ask you some questions about some sections of this. Here is the first one. "Students are told of the theory of intelligent design, ID. Isn't ID simply religion in disguise? No, the theory of intelligent design involves science versus science, where scientists, looking at the same data, come to different conclusions. The theory does not mention or discuss God, Christianity, or the Bible in any way."

Is that accurate?

A. That's exactly right. It's completely accurate.

Q. And another one, "What is the theory of evolution? The word evolution has several meanings, and those supporting Darwin's theory of evolution use the confusion in definition to their advantage. Evolution can mean something as simple as change over time, which is not controversial, and is supported by most people. However, evolution in its biological sense means a process whereby life arose from non-living matter and subsequently developed by natural means, namely, natural selection acting on random variations."

Is that accurate?

A. Yeah, and that sounds clear. I might have phrased things differently but, you know, it's been my experience that people confuse the different meanings of evolution and think that because there's such a thing as change over time, that Darwin's theory might not necessarily be correct. So yes, that seems perfectly fine.

Q. Here's another one. Quote, What is the theory of intelligent design? The theory of intelligent design, ID, is a scientific theory that differs from Darwin's view, and is endorsed by a growing number of credible scientists. ID attempts to explain the complexity of the world by interpreting the scientific data now available to modern biologists. Its principal argument is that certain features of the universe are best explained by an intelligent cause rather than undirected causes such as Darwin's theory of natural selection.

That's the first paragraph in the answer. Do you have any problem with that section?

A. That sounds reasonable.

Q. And then the second paragraph. "In simple terms, on a molecular level, scientists have discovered a purposeful arrangement of parts which cannot be explained by Darwin's theory. In fact, since the 1950s, advances in molecular biology and chemistry have shown us that living cells, the fundamental units of life processes, cannot be explained by chance."

What's your reaction to that section?

A. Well, I think I would have phrased things somewhat differently, but I think for a newsletter, it's fine. It speaks about the purposeful arrangement of parts, which is exactly right, that's the heart of detecting design. So I think it does a good job at getting across the idea.

Q. Now, if something is in a newsletter, would that necessarily be something that you would endorse to be part of a science class or in a science text?

MR ROTHSCHILD: Objection. He has no basis to testify about that. He's making a -- he's asking for a statement about whether this is or is not part of the Dover science curriculum.

MR. MUISE: I don't believe that had anything to do with what my question was, Your Honor. I was asking him about the phrasing of these, whether they would be phrased similarly if he was going to provide similar explanations in a science class or in a science context, would he perhaps do it differently than he would in a newsletter.

THE COURT: Well, he objected to the question as it was framed, because he wouldn't have any basis as an expert -- anybody, I suppose, could give an opinion the way you phrased your question. So I'll sustain the objection, but you might be able to get at it through a different question. You'll have to rephrase.

MR ROTHSCHILD: If the question is, you know, take that same language, is this what you d tell the student -- is this what you d tell the students, I have no objection to the question.

MR. MUISE: That's not my question.

THE COURT: Well, he tried.

MR. MUISE: I'm sorry?

THE COURT: He tried.

MR. MUISE: He can ask that one on cross, Your Honor; this is my witness.

THE COURT: Mr. Muise has the floor, he'll figure it out.

BY MR. MUISE:

Q. Again, Dr. Behe, that last section that I read to you, I believe you testified that you thought that would be fine for a newsletter, is that correct?

A. Yes.

Q. Well, as a teacher of science, if you were going to express something similar to that in a science book or in a science text, would you perhaps word it differently?

A. Yeah, I would rewrite it more carefully, sure.

Q. In terms for a newsletter you believe it's sufficient for the lay person?

A. It, as I said, it gets across that core idea of the purposeful arrangement of parts, which I argued about extensively here. So I -- I think that's the most important point, yes, I think that's good.

Q. And one more, Dr. Behe. Quote, Are there religious implications to the theory of ID? And here's the answer. Quote, Not any more so than the religious implications of Darwinism. Some have said that before Darwin, quote, we thought the benevolent God had created us. Biology took away our status as made in the image of God, end quote, or, quote, Man is the result of a purposeless process that did not have him in mind, he was not planned, end quote, or, Darwinism made it possible to be an intellectually fulfilled atheist, end quote.

Is that question and answer accurate?

A. Yeah, I probably would rewrite that one too. But it certainly is true that scientific theories oftentimes have what people think of as philosophical and theological implications. Philosophers, theologians all the time draw on scientific theories. I think that a number of the experts in this case have written books that impinge on the philosophical and theological aspects of Darwinism. So that's a perfectly -- perfectly correct statement.

Q. Dr. Behe, should school districts such as the Dover Area School District make students aware of intelligent design as a scientific theory during their class instruction of Darwin's theory of evolution?

A. I'm sorry, I missed the question.

Q. I'm sorry. Should school districts such as the Dover Area School District make students aware of intelligent design as a scientific theory during their class instruction of Darwin's theory of evolution?

A. Yes, I think that's a good idea.

Q. And why?

A. Because in order for a student to properly appreciate the difference between fact and theory, one needs at least a couple of different theoretical perspectives to view facts from. If a student is only given one theoretical framework in which to view a theory, then the danger is that the theory will blend into the facts and students will not be able to distinguish the two. Indeed, grown up scientists and philosophers oftentimes have the difficulty.

Additionally, the ability to view a set of facts from a different framework allows a student to judge whether some difficulties for one theory are either greater or lesser. It's been my experience that somebody who is convinced that a theory is true will view difficulties as minor annoyances, or maybe ignore them altogether. But somebody who is not convinced of that theoretical framework might see those difficulties as much more telling and weighty than the first person.

And the third reason is that the strength of evidence supporting a theory, or even whether facts brought to bear have anything to do with a theory, oftentimes depends on a person's theoretical perspective that a person brings to the table in the first place.

Sometimes a person who has a theoretical perspective will view data that is newly obtained as support for the theory, whereas somebody outside of that will think of it as either irrelevant or not -- or not supporting the theory as strongly as the first person.

So I think it's very useful for a student to view data from a number of different perspectives. And so I think it would be good for that purpose.

Q. Does Dover's policy at issue in this case support good science pedagogy?

A. Yes, I think so.

MR. MUISE: Turn over the witness for cross, Your Honor.

THE COURT: All right. Thank you, Mr. Muise.