For those who are interested in what Professor Behe actually said in Dover (instead of the distortions of his testimony in Judge Jones’ opinion)
Thanks to the guys at the Discovery Institute for this...
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. 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.
