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What Behe Actually Said

For those who are interested in what Professor Behe actually said in Dover (instead of the distortions of his testimony in Judge Jones’ opinion), click on “more.”  [Thank you to tribune7 for sussing this out].

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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.
 

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98 Responses to What Behe Actually Said

  1. My pleasure, Barry :-)

  2. FYI, Behe’s background with the histone stuff is irrelevant to the immune system, histones are something completely different.

    I want to get clear on your position. Do you UD folks think that the 58 immune system articles were “good enough”? Do you think Behe thought they were “good enough”?

  3. Nickm writes: “Do you UD folks think that the 58 immune system articles were “good enough”? Do you think Behe thought they were “good enough”?

    You seem to have missed the entire point of this four-day long discussion. My point all along has been that on the record in Dover there is simply no way anyone – including Judge Jones – could tell whether the 58 articles were “good enough” for any purpose whatsoever, much less to impeach Behe’s testimony. There was no expert testimony about what the 58 books and articles said and how they related to Behe’s testimony. And a federal judge is NOT allowed to read them apart from expert testimony and make his own conclusions. He has no training for that task.

    In summary, the 58 books and articles PROVED ABSOLUTELY NOTHING.

  4. In summary, the 58 books and articles PROVED ABSOLUTELY NOTHING.

    Well, they did provide a strong indication that Jones was not a competent judge.

  5. Even if you were right about the legal technicality, which you aren’t, do you really expect the scientific community to take ID seriously, if its response to the scientific literature is legalistic hair-splitting rather than actually dealing with the data? Behe said the scientists had “no answers” to the origin of the immune system in 1996. The well-confirmed transposon model is an answer, so Behe was wrong. Game over for the scientific respectability of ID, until IDers are brave enough to admit Behe was in error here.

  6. Nick,

    The threads about Jones concern the legal aspects of the case. If biology-oriented debate is what you want, why are you posting to them rather than ones such as this about Alan H. Linton’s concerns? You known, the one right below this one?

  7. Behe said the scientists had “no answers”

    Another thing: “probably”, “might” “it seems” “one can imagine”, “should” are not answers.

  8. Nick,

    The threads about Jones concern the legal aspects of the case.

    I guess that explains why neither Nick nor I have been able to discuss the actual published evidence, and no one seems to actually even care to look at it.

    I guess it’s too bad, but thanks anyway for letting us try to steer the discussion that way.

    Cheerio.

  9. Re: Friend of Richard Dawkins interviewed…….

    Sorry about posting here but I cannot find a contact email for your website.

    In New Zealand last weekend we had and ID basher guy on National Radio who is friends with Richard Dawkins. The audio interview is here:

    http://www.radionz.co.nz/audio.....n_williams

  10. Another thing: “probably”, “might” “it seems” “one can imagine”, “should” are not answers.

    Only creationists think it is an actual argument to highlight words like “probably” in scientific articles, because they don’t realize that scientists habitually use tentative language in all their work.

    Deal with the data. Why, apart from the transposon model, should transposon homologs to the RAG genes even exist? Scientists were speculating about the existence of these homologs for years before they were finally discovered in 2005. The only reason scientists looked for those homologs at all was that the transposon hypothesis said that the RAG genes were descended from a transposon. The evolutionary hypothesis is the only reason anyone thought to look for them.

  11. I guess that explains why neither Nick nor I have been able to discuss . . .

    Maybe if you hadn’t mischaracterized Behe’s testimoney you might have been taken more seriously for a serious discussion.

  12. 12

    We can debate these scientific issues until doomsday, but the fact will remain that Judge Jones violated Rule 803(18) of the Federal Rules of Evidence – see
    http://www.uncommondescent.com.....ment-53130

    As Sir Thomas More said in the play “A Man for All Seasons,” “The world must construe according to its wits. This court must construe according to the law.”

    Also, this debate over these complex, contentious, and esoteric scientific questions shows the problems of trying to have such questions decided by a court of law. I feel that the courts should not even attempt to decide such questions unless absolutely necessary for deciding a case, and it was not absolutely necessary in Kitzmiller v. Dover. Judge Jones turned a deaf ear to 85 scientists who filed an amicus brief that urged him to refrain from ruling on the scientific merits of ID and irreducible complexity — this brief said,

    . . . . the scientific theory of intelligent design should not be stigmatized by the courts as less scientific than competing theories . . . . .litigation should not usurp the laboratory or scientific journals as the venue where scientific disputes are resolved. Doubts as to whether a theory adequately explains the evidence should be resolved by scientific debate, not by court rulings. . . . . . Whether or not intelligent design is adopted as an explanation for biological origins, science benefits from the competition of alternate hypotheses. Amici see great value to design theory simply because it forces scientists to confront evidence which conflicts with the Neo-Darwinian paradigm . . . . .
    – from http://www2.ncseweb.org/kvd/al.....ogists.pdf

  13. Why, apart from the transposon model, should transposon homologs to the RAG genes even exist?

    And that is a philosophical question. The scientific — and relevant — one is how did natural selection cause transposons to become RAGs?

    Only creationists think it is an actual argument to highlight words like “probably”

    It’s not an argument. It’s an answer :-)

    Only an atheist could think otherwise

  14. We can debate these scientific issues until doomsday, but the fact will remain that Judge Jones violated Rule 803(18) of the Federal Rules of Evidence

    Larry, good point and good to get us back on topic.

  15. And that is a philosophical question.

    In other words, you don’t have a rebuttal to my point.

    The scientific — and relevant — one is how did natural selection cause transposons to become RAGs?

    Lucky for you, I layed out the basics here:
    http://www2.ncseweb.org/kvd/ex.....b.html#sci

    See the links and references for more…if you dare. So far I have seen very little evidence that you guys follow links to uncomfortable scientific evidence.

  16. 16

    Is anyone else tired of Nick’s arrogance? His absurd statements are just too much. If he’s not claiming (with Andrea) that Behe is a buffoon who gets his scientific info from the NY Times, he’s making silly comments like this.

    Too bad his link doesn’t even begin to answer the question asked! Of course, he has no evidence that natural selection caused transpons to become RAGs. But, he sure can point to the NCSE’s “battle plan” against Behe with claims that A, B, and C maybe, might have, could have, possibly evolved in this manner in this particular possible pathway.

    Reading through the information, links, papers, I guess close is good enough for horsehoes AND science. Well NeoDarwinian views of science, at least,

  17. Nick Matzke wrote:

    So far I have seen very little evidence that you guys follow links to uncomfortable scientific evidence.

    Kind of hard to see evidence if you shut your eyes to it, Nick. I refuted your repeated equivocations. Phyglogeny does not automatically imply Darwinism, and further Behe is not averse to a phylogeny.

    Let me mark this as at least the 3rd time this has been brought to your attention and you’ve repeated the equivocation. Is that the way you do business for NCSE?

  18. OK, Sal, why don’t you tell me why the scientists suspected that a transposon homologous to RAG should exist? The only reason anyone had to suspected its existence is that it was a direct implication of the evolutionary hypothesis that RAG genes descended from a transposon.

    No one at UD has even tried to answer this question yet, even though real science is about testing hypotheses, and this discovery was a dramatic confirmation of the evolutionary model.

  19. Nick,

    As an expert on the case, perhaps you could tell us, or at least provide a link to (I promise I will follow it) a clear explanation of where exactly the 58 articles, etc show how *RM & MS* gave rise to the immune system. This is a great opportunity for you as a member of the NCSE to educate the public on this matter.

    As I am sure you are aware, this is the point Behe has been making all along.

    Thanks,
    antg

    PS I and probably most others here have no problem with RAG genes descending from a transposon. Again as I am sure you are aware, this is not the point in question.

  20. If he’s not claiming (with Andrea) that Behe is a buffoon who gets his scientific info from the NY Times
    This is a blatant mischaracterization (to use a mild expression) of what I, and Nick, said . Anyone reading the original thread can verify this is not true.

    It doesn’t really help your cause to keep insist in this silly accusation.

  21. NickM and/or Andrea

    I don’t dispute descent with modification from one or a few common ancestors. My bone of contention is whether or not it was entirely accidental or proceeded (more or less) by design. I believe the evidence we have so far warrants a design inference.

    In this regard I can’t seem to get an answer to a certain question out of anyone who believes chance and necessity drove the entire process from the beginning to present.

    The question:

    What tests were performed to determine whether the series of mutations that led to the immune system component in question came about by chance or design?

    Silence will be taken to mean no such tests were performed and the presumption of chance is nothing but philosophical/areligous dogma rearing its ugly head in what should be objective scientific inquiry.

  22. NickM:
    Only creationists think it is an actual argument to highlight words like “probably” in scientific articles, because they don’t realize that scientists habitually use tentative language in all their work.

    Only true followers of dogma would accept such words as authoratative truth. Perhaps if people like NickM were as tentative about the dogma he is pushing the world could enjoy OPEN discussions as to the reality of our existence- ie what science should be attempting to answer.

    NickM:
    So far I have seen very little evidence that you guys follow links to uncomfortable scientific evidence.

    So far we have seen little evidence that you EVER plan to substantiate your claims.

    Does NickM even understand the debate?

    Or is he one of the perpetrators of the myth that IC = “it couldn’t have evolved” myth?

    To NickM-

    Do you realize that IC is an argument against the blind watchmaker (ie unintelligent, blind/undirected (non-goel oriented) processes) and NOT an argument against evolution? (yes or no)

    NickM:
    No one at UD has even tried to answer this question yet, even though real science is about testing hypotheses, and this discovery was a dramatic confirmation of the evolutionary model.

    Tell us NickM how would one test the hypothesis that the bacterial flagellum “evolved” via some blind watchmaker-type process from a population (of bacteria) in which not one bacterium had such a structure? Here is your chance but my bet is you either won’t accept the challenge or you will attempt to bluff your way through it.

    To this day I kick myself for not going to the “Kitzmiller” fiasco…

  23. What I absolutely fail to get is how it is possible for people like Nick and Andrea to persist in their incapacity to understand that in fact ID has NO PROBLEM with evolution and even common descent. How is it possible that obviously intelligent people continue to think that every snippet of evidence that change took place is evidence that it took place via RM+NS? Help help help me to understand this bizarre twist in the debate…

  24. Tina, they also persist with the \”Tinkering god\” canard. They seem to be unable to grasp the idea that everything may have been preprogrammed at the very start to unfold at given intervals. With the codes wrapped within codes which we are observing at the molecular level, it just seems silly to me that intelligent people would opt for the primitive notion that only external unguided pressures led to the complexity we see. C\’mon folks, we have new data.

  25. If he’s not claiming (with Andrea) that Behe is a buffoon who gets his scientific info from the NY Times
    This is a blatant mischaracterization (to use a mild expression) of what I, and Nick, said.

    Well, then just be glad I didn\’t allow some of Nick Matzke\’s more offensive comments through the UD filters.

    I had already read the page on http://www.ncseweb.org 2 days ago and my reaction was along the lines of \”that\’s it??\”. Considering the tone of your comments I was expecting much more than a game of connect the dots via imagination. Then again, you\’ve already argued \”much more\” is superfluous…

    As for the main question, there are probably 6 major views:

    1. Evolved via RM+NS.
    2. The RAG genes descended from a transposon via an intelligent process like is suggested with PEH, latent library, etc.
    3. Theistic evolution–not random at all but prescribed.
    4. Tinkering designer.
    5. Designer reuse.
    6. Self-analysis and modification program built into DNA…somewhere.

    Miss anything? I doubt many here would support 1, 3, or 4. Either 2 or 5 is fine with me…6 was just thrown into the list as an act of whimsy. Now everyone can argue about which interpretation is best.

    As for 5: Similarities in different systems are to be expected from an Intelligent Designer when similar functionality design goals are the target. As for RAG1-RAG2 homologs serving a non-immune function in sea urchins…heck, just this last week I was coding some new functionality and borrowed large chunks of code from a function that had a different purpose. Some of my functions are purposely designed to be general purpose so they can be reused all over the place for different types of functionality.

    On a side note, it would be nice if Behe had the time to respond personally (what is he up to nowadays, anyway?).

  26. What I absolutely fail to get is how it is possible for people like Nick and Andrea to persist in their incapacity to understand that in fact ID has NO PROBLEM with evolution and even common descent.

    Tina, I suspect it’s because recurrently one finds statements like this in ID books and at ID web sites:
    http://www.uncommondescent.com.....hives/1446
    in which someone claiming that **there is no evidence for speciation** is quoted approvingly by Wells. And when in that thread I pointed out that in fact even the YECs at AiG accept that speciation occurred, I was accused of “ad hominem” (?), and of “changing the subject”. No one in that thread has pitched in to say that in fact the claim is, by any reasonable interpretation, nonsense.

    And then there is the fact that most of the ID experts who testified in Kansas denied common descent, and that whenever a new transitional fossil is publicized, ID sites are quick to point out that they are not really “transitional”, but “chimeric”, and so on.

    I understand that ID is a Big Tent, but its advocates can’t claim collective immunity from criticism of nutty positions, as long as they are admitted under the tent. At the very least, letting nutty positions in without any sign of internal criticism is a bad indicator as far as scientific rigor goes.

  27. Andrea here is YOUR chance- tell us how to objectively test common descent, as in chimps and humans share a common ancestor. It isn’t that people deny it- It is that people deny there is a way to objectively test the premise and THAT is minus any underlying mechanism.

    And if you want to talk about nutty positions check out evolution #6-

    The meanings of evolution, from “Darwinism, Design and Public Education”:

    1. Change over time; history of nature; any sequence of events in nature
    2. Changes in the frequencies of alleles in the gene pool of a population
    3. Limited common descent: the idea that particular groups of organisms have descended from a common ancestor.
    4. The mechanisms responsible for the change required to produce limited descent with modification, chiefly natural selection acting on random variations or mutations.
    5. Universal common descent: the idea that all organisms have descended from a single common ancestor.

    6. “Blind watchmaker” thesis: the idea that all organisms have descended from common ancestors solely through an unguided, unintelligent, purposeless, material processes such as natural selection acting on random variations or mutations; that the mechanisms of natural selection, random variation and mutation, and perhaps other similarly naturalistic mechanisms, are completely sufficient to account for the appearance of design in living organisms.

    Absolutely nuts especially given what we do know…

  28. 28

    Tribune7 said (comment #6) –
    “Nick — The threads about Jones concern the legal aspects of the case.”

    Andrea replied (comment #8) –
    “I guess that explains why neither Nick nor I have been able to discuss the actual published evidence, and no one seems to actually even care to look at it.”

    Tribune7 replied (comment #11) –
    “Maybe if you hadn’t mischaracterized Behe’s testimoney you might have been taken more seriously for a serious discussion.”

    The reason why Darwinists have been mischaracterizing Behe’s testimony is that they are more interested in defending Judge Jones and the Dover decision than they are in discussing the science. I have yet to see a Darwinist concede that Judge Jones could possibly do anything wrong. The article “Traipsing into breathtaking inanity” on my blog lists many flaws in the Dover decision and court proceedings, and that article does not even get into discussing the scientific issues — see http://im-from-missouri.blogsp.....anity.html My blog also has about ten other articles that denounce Judge Jones.

  29. Oh, so you guys *do* accept the transposon hypothesis? You accept that it is testable and has passed the tests I linked to? I guess the scientific community *does* have an answer then, and Behe was wrong about “no answers.”

    You have no problem with common ancestry? Tell that to Joseph of comment #27. Or have a look at Pandas:

    “Design proponents have a realistic and more cautious approach to the use of homologies. They regard organisms which show great structural differences, such as starfish and chimpanzees, as having no common ancestry.” (p. 127)

    “This is precisely why a book that questions the Darwinian notion of common descent is so necessary. By presenting a reasonable alternative to evolution in this second sense (i.e., common ancestry), Pandas helps students learn to work with multiple perspectives, to distinguish those perspectives from facts, and to guard themselves against the illusion of knowledge.” (p. 156)

  30. Joseph:
    “Andrea here is YOUR chance- tell us how to objectively test common descent, as in chimps and humans share a common ancestor.”

    How about letting a self-proclaimed creationist answer your question:
    http://members.iinet.net.au/~sejones/cmnctsry.html
    In particular, please check out the sections “Vitamin C pseudogene” and “Human-Ape chromosome map (karyotype) comparison”.

  31. Nick

    See the links and references for more…if you dare. So far I have seen very little evidence that you guys follow links to uncomfortable scientific evidence.

    Well Nick, I followed your link, and I was immediately informed of the following.

    “hundreds of PhD scientists have devoted their careers to working out how and why the immune system evolve”

    Wow. That is really amazing. Here is the summary I was given of what those “hundreds of PhD scientists” of come up with for the evolution of the immunoglobulin activation/secretion pathway:

    (1)It begins first with an innate membrane-bound receptor that can induce the transcription and release of antimicrobial peptides upon interaction with a specific foreign antigen (such as LPS).

    (2)A mutation results in an alternative mRNA splice variant that directs the synthesis of a secreted form, providing a selectable advantage.

    (3)Finally, the ability to generate a diverse repertoire of antigen-receptors through gene rearrangement evolves. I can barely make spaghetti in three easy steps but thanks to hundreds of PhD’s devoting their careers the immunoglobulin activation/secretion pathway can evolve in three steps. Of course further detail lets me know that step (3) pretty much is one step.

    Assuming that a non-rearranging antibody-like gene is beneficial, two important components had to appear during the evolution of antibody diversity: the signal sequences and the RAG genes. Their origin is indeed a mystery. … The initial integration event, in one step, inserted both the RAG genes and the RSS sequences, and generated a rearranging antigen receptor.

    Since I don’t have PhD it is possible I have misunderstood the explanation. However, as I read it now it seems like a “hopeful monster” scenerio depending on one big lucky muation.

    As I understand it, the basis of Intelligent Design is the challagne that the complexity in life cannot be achieved by RM+NS. When ID encounters certain complex systems, especially IC systems, it sees an information problem that cannot be overcome by RM+NS. Therefore, pointing to “deep” homologies or phylogenic difference does not overcome the objection that ID raises. Additionally, appeals to “hopeful monsters” and big lucky mutations only strengthens the ID objection.

  32. My last post had some HTML errors and puts my own words in blockquotes. My apologies for any confusion.

  33. Andrea and/or NickM

    No answer for my question in comment 21 about what tests were performed to discriminate between chance and design in the series of mutations leading to the immune system component in question?

    I didn’t think you’d be able to point to any testing in that regard. I was hoping one of you would at least show enough intellectual honesty to admit it. There’s still time. I’ll presume you missed the question.

    And since this thread is about what Behe actually said I’ll point out that Behe accepts descent from one or a few common ancestors as a reasonable position. He may harbor some measure of doubt but it’s not a lot. I too harbor some measure of doubt but it’s very little. The fossil record, molecular homology, common genetic code, and the observation that life always comes from life, are enough to convince me beyond reasonable doubt that common ancestry is true. But it’s an inference and as such there must always remain some measure of uncertainty. Design is also an inference and for me there is more doubt about it but I think it’s the best explanation for the origin of the first cell using DNA and ribosomes. The chance formation of digital program and data code that drives a protein assembly machine like a factory robotics system is just too much for me to swallow without a plausible explanation for how it was possible. If that can be demonstrated I’m willing to concede everything that followed was driven by chance as well. Absent such demonstration, design of the first cell by an unknown agent or agency, remains a live possibility. And if the first cell was designed it also remains a live possibility that the original genome was not simple but rather very complex and contained all the information needed to diversify along a more or less preset path with chance playing little if any role in the diversification much as a fertilized egg cell has all the information to diversify into all the myriad different cells and organization that makes a human being.

  34. By Jehu:
    “Since I don’t have PhD it is possible I have misunderstood the explanation. However, as I read it now it seems like a “hopeful monster” scenerio depending on one big lucky muation.”

    I think some of the people here may have some misconceptions about how science proceeds. The transposon hypothesis began in 1979 when the Tonegawa lab sequenced the immunoglobulin genes and found sequences that resembled the ends of transposons. They asked the question of whether or not the V(D)J recombination system may have arisen from a system similar to transposons. If the V(D)J recombination system evolved from a transposon, what features would be expect to find in the V(D)J recombination system? The subsequent experiments in the last 25 years on that issue were inspired by that question.

    Think to yourself, what would we expect to find? Well, at that point, the RAG genes hadn’t been discovered yet, so one prediction based on that model was that the RAG genes were transposases. When the RAG genes were discovered, their genomic organization was very similar to transposons (two genes, tightly clustered, no introns). A few years later, it was discovered that RAG genes had transposase activity, first in the test tube, then evidence was found in organisms. Remember, Behe specifically mentioned the RAG genes and V(D)J recombination in Darwin’s Black Box. He said that components of IC systems would not be found outside of the IC system (unless they evolved FROM the IC system, as is argued for the Type III secretory systems). However, in contrast to Behe’s predictions, we found RAG genes outside of mammals, in organisms that have nothing that resembles an adaptive immune system.

    Now does this satify Behe’s requirements for an answer? Probably not, nor will it ever. But every other immunologist considers the transposon origin model essentially proven precisely because of the wealth of evidence that’s been accumulating for the last 25 years on it. There’s been no result that seriously undermines this model.

    It may help to think of this like a murder investigation. We have a prime suspect, and we hypothesize that he is the killer. We ask, what would the evidence be if our prime suspect was the killer? We find that the killer was left handed, between 6’1″ and 6’4″, was blood type O, and had blonde hair. We find that the prime suspect had all those features. Certainly there are many people out there that would fit that description, but then we find the suspect had no alibi, and that he would have profitted tremendously by that person’s death. Again, more and more evidence points to him. We then find that he owns a gun, and the bullet drawn from the victim matches his gun. Furthermore, ballistics shows that the bullet has the same markings as a bullet fired from the suspect’s gun. What we see in this example is a steady accumulation of evidence all pointing to a single conclusion, that the suspect is the killer. Would a jury insist on a moment-by-moment account of the suspects exact whereabouts the night of the murder? Would they demand proof that the suspect fired that gun on that night? There are a million ways a jury can nit-pick the case, and a defense lawyer can invent alternative theories with no evidence for them whatsoever, but when is enough enough? The community of immunologists has been following this case for a long time, and they all agree, the transposon model is without doubt the current, best explanation for the origin of the V(D)J recombination system.

    Of course, all the evidence has already been linked to, again and again. It’s there if anyone is interested in looking at it and discussing it.

  35. Since I don’t have PhD it is possible I have misunderstood the explanation. However, as I read it now it seems like a “hopeful monster” scenerio depending on one big lucky muation.

    Except that transposition occurs all the time, and diversity in immune receptors is positively selected for in a wide variety of critters. It’s not all that remarkable really. The gene rearrangements that produced the modern VDJ system are mostly quite standard processes of duplication etc. For more detail see this 2000 review paper, also linked: http://www.jem.org/cgi/content/full/191/10/1631 …not completely up to date but quite useful.

    You were quoting Matt Inlay’s 2002 essay, note that since then they have found the homologs of the ancestral receptor and the hypothesized transposon, which were a “mystery” in 2002. Surely the evolutionary immunologists deserve some credit for that.

    Regarding the various questions about how to test your alternative explanation, a design model that somehow involves the transposon the evolutionary biologists predicted and discovered — I could give you my thoughts, but you have to actually present a design model first. But once you’ve reached this point, you are now arguing something different: “ID can explain the data too” — which concede that evolution already provided an answer, which is exactly what Behe denied.

  36. 36

    Chance played no role whatsoever in either the origin or origins of life, its subsequent phylogeny or its present ontogeny which is all that remains.

    “Neither in the one nor in the other is there room for chance.”
    Leo Berg, Nomogenesis, page 134

    The idea of a predetermined (prescribed) evolution is not new and can be traced back to Bateson:

    “Finally, Bateson likewise (1914, page 640) inclines to the view that the entire process of evolution may be regarded as an ‘unpacking of an original complex which contained within itself the whole range of diversity which living things present.’”
    Leo Berg, Nomogenesis, page 359

    Intelligent Design by elements far beyond our comprehension, in my view, is not an inference, but a mandatory starting point without which nothing in the inanimate or animate world will ever make any sense. Phylogeny is the perfect model for phylogeny. Both have always proceeded on the basis of contained initial information and the only role for the environment was that of providing a stimulus. The usual stimulus for the development of the egg is penetration by the sperm which can be substituted for with a needle. The male haploid nucleus is quite unecessary and for many forms it provides no information anyway, serving only as an activating agent. These are not surmises but experimentally verified conclusions. I believe that the spermatazoon initially was an activator only, which later, with the several independent inventions of sexual reproduction, became a contributor of genetic information. With mandatory sexual reproduction, all creative evolution ceased which is why it cannot be demonstrated today. Sexual reproduction, allelic mutation and natural selection are all conservative anti-evolutionary devices. Accordingly, Mendelian genetics had nothing to with with creative evolution either. All it can manage is the creation of subspecies and varieties neither of which are incipient species. Bateson realized this too as I presented elsewhere here at Uncommon Descent as well as in published hard copy.

    The truth lies elsewhere and I think it lies in the Semi-meiotic hypothesis (SMH) which still awaits testing with suitable material. Like all hypotheses it remains viable until found to be inadequate. Don’t expect Darwinian laboratories to undertake these experiments as they quit testing their own hypothesis decades ago. Actually Darwinism has never been an experimental science anyway and to that extent Darwinians are not scientists! Certainly none of their recent spokespersons are or were, Richard Dawkins, Stephen J. Gould and Ernst Mayr, all of whom retired early, became glued to their endowed chairs and dedicated the rest of their lives to book after book extolling the atheist Darwinian fairy tale.

    So much for Darwinism.

    It is hard to believe isn’t it?

    I love it so!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  37. Nick

    Except that transposition occurs all the time, and diversity in immune receptors is positively selected for in a wide variety of critters. It’s not all that remarkable really.

    We are not talking about a mere unremarkable transposition. We are taking about an alleged “initial integration event” which, “in one step, inserted both the RAG genes and the RSS sequences, and generated a rearranging antigen receptor.” This is what I mean by a “hopeful monster” or “one big luck mutation.” It has been noted that such arguments are no different than appeal to miracle. (abiogenesis for example)

    The gene rearrangements that produced the modern VDJ system are mostly quite standard processes of duplication etc. For more detail see this 2000 review paper, also linked: http://www.jem.org/cgi/content/full/191/10/1631

    I reviewed your paper. As you noted it was written in 2000, anyway it doesn’t seem to give the detail you suggested. Note in the summary it states:

    It remains to be pointed out that some of the most extensive changes that have occurred during the evolution of Ig and TCR loci cannot be explained by some combination of the operations shown in Fig 2. The conversion of “cluster” type loci to the “extended” form is not easily understood, nor is the huge variation in multiplicity of gene segments at different loci, or the manner in which, for some loci, gene segments were first flipped into an opposite transcriptional orientation.

    What we IDists are interested in is how you cross the huge information barriers necessary to construct complex and IC systems. Again, pointing to “deep” homologies and “hopeful monsters” only strengthens the ID case. If there is an explanation for how these information barriers are crossed you still have not demonstrated it.

  38. John A.

    You like to repeat that “Chance played no role whatsoever in either the origin or origins of life, its subsequent phylogeny or its present ontogeny which is all that remains.”

    Did mass extinctions like the dinosaur happen by chance?

  39. By Jehu,
    “We are not talking about a mere unremarkable transposition. We are taking about an alleged “initial integration event” which, “in one step, inserted both the RAG genes and the RSS sequences, and generated a rearranging antigen receptor.” This is what I mean by a “hopeful monster” or “one big luck mutation.” It has been noted that such arguments are no different than appeal to miracle. (abiogenesis for example)”

    Except the “intial integration event” IS an unremarkable transposition event. Our genomes are littered with the remnants of transposons. Transposition happens all the time. No one here is appealing to miracles, just probability. If there’s a one in a million chance of a transposon inserting into an antigen receptor gene, and a population of millions of organisms undergoing transposition reactions, the transposon origin model becomes entirely plausible.

    From the 2000 JEM paper:
    “The conversion of “cluster” type loci to the “extended” form is not easily understood, nor is the huge variation in multiplicity of gene segments at different loci, or the manner in which, for some loci, gene segments were first flipped into an opposite transcriptional orientation.”

    All of those features could have come about through gene duplication and recombination. There’s really nothing controversial about those features, and they have nothing to do with the origins of V(D)J recombination.

    By Jehu,
    “What we IDists are interested in is how you cross the huge information barriers necessary to construct complex and IC systems. Again, pointing to “deep” homologies and “hopeful monsters” only strengthens the ID case. If there is an explanation for how these information barriers are crossed you still have not demonstrated it.”

    The “huge information barriers” are crossed by generating a model for the origin of a system, making predictions based on that model, then testing the predictions. Basic run-of-the-mill scientific method stuff. The experiments presented in the 58 publications, and summarized in the links Andrea and Nick have posted, describe in vivid detail that process. Again, for the 3 part V(D)J recombination system, we can find organisms that possess each of these parts in separate subsystems, all of which are functional (though they don’t possess the same function as the V(D)J system). As all of these parts were discovered in the last few years, their existence had been predicted for quite some time.

    Incidently, I don’t see how pointing to homologies strengthens the ID case. You seem to be saying that the strength of ID rests not upon the strength of its own evidence but the supposed insufficiency of the evidence for evolution. Do you really want to make that claim?

  40. Nick Matzke asked:

    OK, Sal, why don’t you tell me why the scientists suspected that a transposon homologous to RAG should exist?

    The V(D)J reaction bore similarity to a transposon reaction.

    But the quesiton of similarity of function or similarity of architecture is not what is in question by Behe or IDers. The question of co-option is not just the availability of parts, but the step by step evolution of the integrated system in terms of selection pressures, and population resources, and many other factors.

    Now that I have attempted to answer your question, will you answer one of mine.

    Do you recognize that your version of what constitutes “detailed and testable” is not the same as what Behe constitutes as “detailed and testable”?

    Salvador
    PS
    I tried posting to one of your threads at PT on the poll of 34 countries, did I get trapped in the spam buffer?

  41. minlay,

    I don’t see how pointing to homologies strengthens the ID case. You seem to be saying that the strength of ID rests not upon the strength of its own evidence but the supposed insufficiency of the evidence for evolution. Do you really want to make that claim?

    You are correct on this point. I badly mangled an attempt to paraphase my previous statement.

    Therefore, pointing to “deep” homologies or phylogenic difference does not overcome the objection that ID raises. Additionally, appeals to “hopeful monsters” and big lucky mutations only strengthens the ID objection.

    I still stand behind this assertion.

  42. Minlay, “I don’t see how pointing to homologies strengthens the ID case.”

    Actually there are some homologies that demonstrate a stark lack of opportunism within nature, a lack of opportunism which is not suggested by the NDE theory. I point, in particular, to pentadactylism. There is not a single living species of quadruped whose prototype is polydactyl. Yet it has been demonstrated in mice, cats, dogs and humans that polydactylism is a single non-destructive mutation away. In “Eight Little Piggies”, Gould suggests that this is an important puzzle meriting research. He, honest evolutionist that he was, suggests that his science can find no reasonable explanation for this lack of variety.

    Jehu might not, but I contend that homology is much too consistent a phenomenon to be reasonably explained by NDE.

  43. Minaly

    Except the “intial integration event” IS an unremarkable transposition event. Our genomes are littered with the remnants of transposons. Transposition happens all the time.

    Transpositions, which, “in one step” insert “both the RAG genes and the RSS sequences” and generate a “rearranging antigen receptor” do not happen all of the time. This seems like a rather implausibly fortituous event.

    No one here is appealing to miracles, just probability.

    One word. abiogenesis

    If there’s a one in a million chance of a transposon inserting into an antigen receptor gene, and a population of millions of organisms undergoing transposition reactions, the transposon origin model becomes entirely plausible

    Well if it is that probable why don’t you just set forth the detailed explanation of the step by step evolution of the integrated system including needed selection pressures, population resources, and the other relevant factors.

    Or better yet, if you want to prove Behe wrong, point to this explanation within the 58 references he was presented with.

  44. bFast:
    “There is not a single living species of quadruped whose prototype is polydactyl. ”

    You mean you won’t accept the panda’s thumb as an extra finger? ;)

  45. By Jehu,
    “Transpositions, which, “in one step” insert “both the RAG genes and the RSS sequences” and generate a “rearranging antigen receptor” do not happen all of the time. This seems like a rather implausibly fortituous event.”

    It seemed a lot more implausible a few years ago, before the RAG genes were discovered in a transposon, or before it was known that the RAGs had transposase activity, or before an antigen receptor without RSS sequences were discovered. A Rag gene flanked by RSS sequences IS a transposon. A transposon inserting into any gene is not implausible. If you have a million jawless vertebrates, and each one has a transposon insertion, then the odds are pretty good that in one of those organisms, the transposon will insert into an antigen receptor gene. That isn’t implausible.

    “Well if it is that probable why don’t you just set forth the detailed explanation of the step by step evolution of the integrated system including needed selection pressures, population resources, and the other relevant factors.”

    Because those demands aren’t necessary to demonstrate the robustness of evolution. What you’re asking for is absolute proof. That’s not how science proceeds. We have a ton of data, it all supports the transposon model. That’s as much as you can ask for any biological system. If you don’t feel that’s enough, then try to apply those standards equally to ID. Evolution is vastly more detailed and vastly more testable than any model of ID. Why the double standard?

    “Or better yet, if you want to prove Behe wrong, point to this explanation within the 58 references he was presented with.”

    The problem here is that Behe’s concept of what constitutes strong evidence for the evolution of a system isn’t very good. If you take what he says at face value, that “the scientific literature has no answers to the origin of the immune system”, then he’s very much mistaken, as the 58 articles demonstrate. However, if you redefine the word “answer” to be absolute, definitive, proof, as he has done, then they don’t meet that requirement. What Behe has failed to do is show WHY evolution is required to be demonstrated to such absolute certainty as he demands. Again, there’s a ton of data out there, and it all supports one model. If Behe or anyone else wants to propose an alternative model and see how it stacks up to the data, they’re more then welcome to try. However, no one out there is trying to develop an ID origin for the immune system, or any other IC system, that is both detailed and testable.

  46. ofro, “You mean you won’t accept the panda’s thumb as an extra finger?”
    In “Eight Little Piggies” Gould goes on extensively about the panda’s thumb. The panda’s thumb is not a “true finger” from Gould’s perspective, but an extension of one of the bones in the hand. What the panda’s thumb does, however (again according to Gould) is show that a sixth digit can prove sufficiently valuable that mechanisms are found to create it — even though the panda would also likely grow an extra finger with just a single mutation.

    Though Gould died as a neo-Darwinist, he certainly was honest about weaknesses in the theory. He had a penchant for denegrating “ultra-Darwinists”. It is my understanding that Gould suggested that a pattern of DNA coding for multiple proteins would be the death nell to the theory. It is my understanding that since his passing, it has been discovered that the average segment of coding DNA codes for 5 different protein configurations. I wonder if this would have been evidence enough to cause him to abandon the neo-Darwinian camp.

  47. minlay,

    If you have a million jawless vertebrates, and each one has a transposon insertion, then the odds are pretty good that in one of those organisms, the transposon will insert into an antigen receptor gene. That isn’t implausible.

    Then why don’t all organisms have such immune systems, if it is so probable? I really don’t think you have any idea what the odds are or what the steps are, otherwise, you would specify them. Instead cite “deep” homology to a transposon and wah-lah!

    Because those demands aren’t necessary to demonstrate the robustness of evolution. What you’re asking for is absolute proof. That’s not how science proceeds. We have a ton of data, it all supports the transposon model.

    You mean because you can’t. You have no clue. If someone says the information leap is too great to cross by RM+NS, you just point to the “deep” homology to transposons and then try to literature bluff the rest. As for your “deep” homology, it only supports the transposon model if you assume the immune system was created by RM+NS and it doesn’t show whether the information gap could be crossed.

    You believe without proof, even in the face of the problem of novel information. How is that different than faith?

  48. I’m loving this thread! It’s clearly worth the price of admission.

    Minlay and ofro, thank you for your even-keeled presentations of Darwinism. Jehu and bFast, you keep hitting those fastballs out of the park!

    If Scott Adams could have seen threads like this, there would be no such thing as the “Dilbert principle” in this debate!

  49. bFast:”In “Eight Little Piggies” Gould goes on extensively about the panda’s thumb.”

    Sorry, I was pulling your leg (pun intended). I thought you would reconized my smilie. I am aware of Stephen Gould’s essay on the panda’s thumb and thought it was brilliant. (And too bad my name isn’t Steve).

    “It is my understanding that since his passing, it has been discovered that the average segment of coding DNA codes for 5 different protein configurations.”

    On a serious note, nature is even stranger than Gould imagined. What you presumably are referring to is that many genes give rise to different proteins through alternative splicing (i.e during RNA processing, when the introns are removed, one or the other exon can be removed as well, eventually yielding different proteins that differ in their presence or absence of stretches of amino acid sequence.) What is even more fascinating is that in bacteria the same stretch of DNA is read in more than one open reading frame(i.e. the start of translation into an amino acid is shifted by one nucleotide, which results in different triplet codons and therefore a copletely different amino acid sequence. So one “gene” has two totally different gene products. I know of at least one mammalian case as well, where omission of an exon results in the shift of the downstream an open reading frame and in two different peptides, both of which with apparent function.

    HOwever, I stringly believe that Stephen Gould would have accepted the notion of a gene resulting in multiple gene products as being consistent with his Darwinian framework.

  50. To Ofro,

    I read S Jones. I don’t see how that is a test for common descent nor do I see how it is objective. He also says that it isn’t “evolution” if the processes aren’t unintelligent, blind/ undirected.

    The ONLY way to truly test common descent is by knowing what makes an organism what it is and then we can test to see whether or not one population could (or could have) “evolve” into another.

    1. Vitamin C pseudogene as evidence for common ancestry-

    At first glance this “argument” appears sound, but a closer look reveals something much different. First of all the mere persistence of this (any) DNA sequence would suggest anything other than “pseudo”. True it may not code for an amino acid sequence, but if it served no function at all why would it persist intact enough for so many generations as to be used as some kind of hereditary marker all the while other genetic changes are (allegedly) occurring elsewhere in the same genomes that allow for profound morphological change- ie the morphological differences between chimps and humans?
    What needs to be explained are not the apparent similarities but the obvious differences. For example CAN changes in DNA, “the stuff of heredity” allow for the differences- upright bipedal walking,

    Genetic similarities could also point to a common design. What evolutionism needs to explain and has not explained are the differences. Why? Because even though some genes have some differing sequences the protein products are the same and perform the same functions. So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?

    NickM:
    You have no problem with common ancestry? Tell that to Joseph of comment #27.

    I have no problem with that NickM. Just as long as it is acknowledged that CD is accepted on faith because no one can demonstrate how to objectively test the premise.

    Ofro:
    The problem here is that Behe’s concept of what constitutes strong evidence for the evolution of a system isn’t very good.

    That is because what is presented isn’t very good.

    Ofro:
    What Behe has failed to do is show WHY evolution is required to be demonstrated to such absolute certainty as he demands.

    As I have already posted- because without that level of knowledge no one can reject the design inference a priori- that is if science is about the search for the reality to our existence.

    Ofro:
    Again, there’s a ton of data out there, and it all supports one model.

    That is nothing but wishful thinking. Obviously it supports more than one model as there are many scientists who are either TE’s or IDE’s. Then there are those scientists who are Creationists.

    Ofro:
    However, no one out there is trying to develop an ID origin for the immune system, or any other IC system, that is both detailed and testable.

    What would you accept? If Behe went into the lab and designed an immune system would that make it OK to put ID in a science classroom?

    The point of the design inference is that we have observed intelligent agencies design and build them. We have never observed unintelligent, blind/ undirected (non-goal oriented) processes do that. Therefore if someone is claiming that an IC structure arose by the blind watchmaker the onus is one them to substantiate the claim.

    I would love to see a blind watchmaker develop alternative gene splicing. That discovery alone should have refuted the blind watchmaker thesis.

    Ofro:
    We have a ton of data, it all supports the transposon model.

    And once again-

    Dr. Spetner discussing transposons:

    The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism [I]random[/I] before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.

  51. By their silence, the NDE defenders have admitted there were no tests performed to discriminate between chance and design. Why then, in the absence of supportive evidence, do we teach our children that evolution was a purposeless process with no predetermined outcome? The answer is simple. Evolution by chance and necessity is not science. Evolution by chance and necessity is dogma. Axiomatic. Faith based. A godless religion. Science is agnostic and evidentiary. Science is about the demonstrable not the mythical. If there are things it cannot answer because of lack of evidence then there’s a mystery. Darwin of the Gaps is no more scientific than God of the Gaps. Gaps is gaps.

  52. 52

    In response to message #38, I will defer to Einstein.

    “Everything is determined… by forces over which we have no control.”

    That which IS determined most certainly must HAVE BEEN determined. I see no reason why that could not include the extinction of the dinosaurs. After all, the giant Amphibians suffered the same fate didn’t they? Before them the Crossopterygians, the Trilobites etc, etc. Need I go on? Without extinctions evolution could never have occurred. Like Einstein, I too will die a convinced determinist. Do you want to make something out of it? You better hurry as I am not getting any younger. Why don’t you publish your views as I have? The internet is so ephemeral don’t you know. It is little more than catharsis typically presented by anonymous authors, a policy I have always opposed. Posters would be more cautious if their identity was at stake. Anonymity is lttle more than licence for unbridled abuse and denigration as I can surely testify.

    I have no idea who you are and really don’t care anyway. If you should decide to reveal your identity and credentials I might take you seriously. Then again I might not!

    “A past evolution is undeniable, a present evolution undemonstrable.”
    John A. Davison

  53. Joseph:
    “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?”

    The reason is that the mutations can not only affect a protein’s function but also its expression level. For example, much if not most of embryological development relies on the proper expression level of a whole bunch of transcription factors. As we know now experimentally, many transcription factors are readily exchangeable between different species without noticeable consequences to development. However, what is different in different species is the “activity” of the promoter, i.e. slight differences in the DNA sequence of a promoter region determine how long a transcription factor remains bound and therefore maintains expression of a desired protein.

    The consequences can be more or less subtle. In birds, the expression level of a protein called calmodulin apparently can influence the shape of its beak (see http://www.nature.com/nature/j.....04843.html). So many appearances (body hair, skin color, etc.) as well as morphologically invisible but nontheless obvious phenomena (extent of neuronal connectins in the brain) depend on expression levels, not on different protein function. There are many diseases where it is not the protein that is “at fault” but its promoter.

    I hope that answered your question.

  54. “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?”

    Ofro:
    The reason is that the mutations can not only affect a protein’s function but also its expression level.

    But the function is not affected. And the changes you relate to in no way relate to the changes required by common descent.

    Ofro:
    I hope that answered your question.

    It does if we were discussing variations within a population. However we both know we aren’t discussing that.

    What makes a fly a fly? In his book (English title) “Why is a Fly not a Horse?”, the prominent Italian geneticist Giuseppe Sermonti, tells us the following :

    Chapter VI “Why is a Fly not a horse?” (same as the book’s title)

    “The scientist enjoys a privilege denied the theologian. To any question, even one central to his theories, he may reply “I’m sorry but I do not know.” This is the only honest answer to the question posed by the title of this chapter. We are fully aware of what makes a flower red rather than white, what it is that prevents a dwarf from growing taller, or what goes wrong in a paraplegic or a thalassemic. But the mystery of species eludes us, and we have made no progress beyond what we already have long known, namely, that a kitty is born because its mother was a she-cat that mated with a tom, and that a fly emerges as a fly larva from a fly egg.”

    When you or anyone else can demonstrate differently I will be all ears.

  55. By Jehu,

    “Then why don’t all organisms have such immune systems, if it is so probable? I really don’t think you have any idea what the odds are or what the steps are, otherwise, you would specify them. Instead cite “deep” homology to a transposon and wah-lah!”

    All organisms do have immune systems, each of them functions in its own right. There’s no reason to think they’d all have the same immune system.

    Scientists who study the evolution of the immune system aren’t interested in calculating probabilities. They generate models and test those models. If you don’t think that’s enough, then you’re questioning the entire scientific method. What you describe as ‘wah-lah’ are predictions of the model verified empirically. Can ID boast similar success?

    “You mean because you can’t. You have no clue. If someone says the information leap is too great to cross by RM+NS, you just point to the “deep” homology to transposons and then try to literature bluff the rest. As for your “deep” homology, it only supports the transposon model if you assume the immune system was created by RM+NS and it doesn’t show whether the information gap could be crossed.”

    It’s unfortunate you result to insults to make your points. Why do you say the information leap is too great to cross? Because Behe says so? If the immune system is too complex to evolve, then why is there paper after paper verifying predictions of the model for its evolution? All I’m hearing now is a demand for infinite knowledge, but that’s not how science works. Do you agree that there’s utility in the scientific method, the process of model-forming and model-testing?

    You can nit-pick the transposon model all you want, but the fact remains, there are tons of experiments based on that model, and tons of data that supports it. Where are the ID experiments? Where are the “detailed” and “testable” models for the origin of an IC system by intelligent design? It seems very hypocritical to demand absolute proof of evolution, when no one here is demanding such rigor from ID.

    “You believe without proof, even in the face of the problem of novel information. How is that different than faith?”

    Because absolute proof is a myth in biology. There’s no system in biology for which there is absolute proof of its workings. The only thing I have faith in is that the scientific method is the best method we have for discovering how our world works. If you have a better method, by all means present it. I’d love to hear it.

  56. DaveScot writes,

    “By their silence, the NDE defenders have admitted there were no tests performed to discriminate between chance and design.”

    No design model has been offered for the origin of VDJ recombination, despite my requesting this. Behe couldn’t do it when asked at trial, and you guys can’t do it here.

    Sal still doesn’t get that the whole point of the immune system literature stack at trial was specifically to show that Behe’s version of “detailed and testable” was ridiculous and unreasonable, and that he was only maintaining his claims about IC by waving away massive amounts of evidence with his unreasonable criterion.

    You have to chose, Sal. Shall we require all science to provide near-infinite detail before any model is accepted? (Like Behe requires for evolution) Or, instead of omniscience, shall we go with the standard science has successfully used for hundreds of years, namely, testable models and passed tests?

    Which one is the reasonable standard, Sal?

  57. Nick,
    Your claim that Behe was asking for near-infinite detail is specious rhetoric. What is “near-infinite”?
    The detail Behe has asked for has been discussed, and is indeed finite. It is the kind of detail that is required by any other science making claims of a mechanism’s ability to create a result – step by step testable models or experiments showing that the claims are actually being demonstrated, including relevant variables. This is surely not too much to ask of a science whose claims are to be taken as ‘fact’, which are as well-attested to as gravity, and which are as proven as the claim that the Earth revolves around the sun.

    If the prosecution had as its intent to show that Behe’s standards are not scientific then they would have produced experts who said “no, in science we do not rely upon testable models or experiments which show that mechanisms can account for what we say they can”. What the prosecution was really trying to do, as they asked the question many times over the several sessions, was to impeach Behe on his claim that there is no detailed account in the literature of how complex molecular systems can arise by a Darwinian mechanism. Their literature bluff was an attempt to show that he had lied, or was ignorant, on this subject, and that he was now raising his standards too high so as to wave away his error. As we saw in the last thread, however, his standards were never raised and the goal posts were never shifted.
    Behe’s claim has always been the same and his opponents and Rothschild knew what they were all along.
    They could have demonstrated that his requirements were unscientific, but chose instead to grandstand.

  58. Minlay:
    Where are the ID experiments?

    If Dr Behe went into a lab and designed a bac flag would that make ID true?

    NickM:
    Sal still doesn’t get that the whole point of the immune system literature stack at trial was specifically to show that Behe’s version of “detailed and testable” was ridiculous and unreasonable, and that he was only maintaining his claims about IC by waving away massive amounts of evidence with his unreasonable criterion.

    But THAT is exactly the same level that you expect from IDists BEFORE ID can be even considered.

    OK NickM- just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?

    Where is THAT in your literature?

  59. But THAT is exactly the same level that you expect from IDists BEFORE ID can be even considered.

    On the contrary. One demonstrated example of the intelligent designer mucking around, at one instant, (with photos, preferably) would be enough to validate the ID hypothesis. Behe is asking that it be proved that the laws of nature, which have been rather remarkably consistent in the realm of scientific observations, were *never* trespassed upon by the designer during the rise of one of his complex systems.

    To the extent that ID claims that there is direct proof that the designer did something, it is to ID to demonstrate the claim (as Dembski, to his credit, has attempted, though by indirect means).

    If all ID is saying is ‘a supernatural designer _might have_ done something’, I don’t think much of anyone would care to refute the claim.

  60. Charlie, you do realize that Nick was at the trial, and helped the prosecution develop their strategy?

    I consider a mutation-by-mutation account of the evolution of an entire system to be “near-infinite”. Do we need a day-by-day account of the whereabouts of a historical figure to be fairly certain that he or she existed? Why don’t IDists demand a step-by-step pathway for how the intelligent designer created the immune system?

    Do you have an alternative explanation for why the RAG genes STILL retain transposase activity, when their primary function is recombination? Or why both the RAG-1 and RAG-2 genes contain no introns, and are located adjacent to each other in every genome they’ve both been found in? Or why the RSS sequences are nearly identical to the sequences that flank numerous transposons? These are discoveries that are not only consistent with the transposon model, but were also predicted by it. If there’s an ID model that can incorporate these findings, and can make future predictions, then we’d all love to hear it. Until then, how would you interpret that data?

    I’m not going to lie to you and say that the transposon model is 100% certain. I think in order to do that, we would probably need data very similar to what you’ve been demanding. However, we have some very strong data to support that model, and we can be fairly certain that the basic idea of the transposon model, that the V(D)J recombination system evolved from a transposon, is correct. And our certainty increases every year as new data is discovered. So yes, there is some uncertainty, but I don’t see how you can take that uncertainty and interpret it to mean that there is NO evidence for the evolution of that system, and further still, that ID is a BETTER explanation.

    (my formating would be better if I could find the formating instruction page)

  61. Minlay,

    One more time

    The debate is NOT whether or not some structure/ system could have evolved. The debate is about the mechanism. NickM doesn’t understand that. Andrea doesn’t understand that. And now it is apparent that YOU do not understand that.

    And again the design inference exists because in EVERY case in which we know the cause and IC and/ or CSI is present, both are ALWAYS the result of an intelligent agency. Couple that knowledge with the fact we have NEVER observed unintelligent, blind/ undirected (non-goal oriented) processes bringing forth IC or CSI.

    Relying on transposons is a sure sign you have given up on any blind watchmaker thesis.

  62. Matt.

    Charlie, you do realize that Nick was at the trial, and helped the prosecution develop their strategy?

    Yes I do. Thank you for putting such a fine point on it for anyone who might not have been aware of Matzke’s intimate involvement with the strategy that we are so harshly criticizing. By the way, I am criticizing it not as a legal or rhetorical strategy, but as one representing truth. I think the cross-examination was quite brilliant, but that Behe was more than up to it.

    I’m not going to lie to you and say that the transposon model is 100% certain. I think in order to do that, we would probably need data very similar to what you’ve been demanding.

    Thank you, and thank you.

    So yes, there is some uncertainty, but I don’t see how you can take that uncertainty and interpret it to mean that there is NO evidence for the evolution of that system,

    That’s not the point, was not Behe’s point, was never Behe’s point, and was not refuted by the literature bluff. See Joseph above.

    and further still, that ID is a BETTER explanation.

    See Joseph above.
    Thanks, Joseph and Matt.

  63. By Joseph,
    “The debate is NOT whether or not some structure/ system could have evolved. The debate is about the mechanism. NickM doesn’t understand that. Andrea doesn’t understand that. And now it is apparent that YOU do not understand that.”
    That’s exactly what we’re discussing here. The transposon model is based on the mechanism of RM/NS. Transposition is a form of random mutation. It IS the mechanism.

    “And again the design inference exists because in EVERY case in which we know the cause and IC and/ or CSI is present, both are ALWAYS the result of an intelligent agency.”

    Do you really consider that evidence compelling? How many of those IC objects whose causes were discovered were biological organisms? How many of the intelligent agents were non-human? What evidence do you have that an intelligent designer even existed 500 million years ago? Have you ever seen an archaeologist propose a non-human origin for a rock in the shape of an arrowhead? Have you ever seen forensic scientists look at a crime scene and deduce a non-human culprit for an intelligently designed crime? All your design cases were caused by humans.

    “Couple that knowledge with the fact we have NEVER observed unintelligent, blind/ undirected (non-goal oriented) processes bringing forth IC or CSI.”

    But there is no logical barrier to the evolution of IC systems, and we have a ton of evidence to suggest that IC systems can and do evolve. We certainly have more evidence of that than IDists have that a designer existed back then.

  64. Charlie, as you can tell by my response to Joseph, I don’t think that that logic is very sound. Maybe you can elaborate a little more on the ID inference for me. What research do you think can be done to further this ID model of origins? Do you consider the study of human-designed objects as something that can further ID?

  65. Minlay:
    That’s exactly what we’re discussing here. The transposon model is based on the mechanism of RM/NS. Transposition is a form of random mutation. It IS the mechanism.

    Transposition is a form of random muation? How was that figured out?

    Dr. Spetner discussing transposons:

    The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism [I]random[/I] before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.

    the same people who call that random are also the same people who claim that life arose from non-living matter via random shuffling of elements.

    As far as we know transposition of genetic elements are as random as statements in C++ programs. For example someone who didn’t understand C++ would think that “go to” “if else”, etc. were random events. C++ programmers know better.

    “And again the design inference exists because in EVERY case in which we know the cause and IC and/ or CSI is present, both are ALWAYS the result of an intelligent agency.”

    Minlay:
    Do you really consider that evidence compelling?

    Gee I guess I stand refuted. LoL! But anyway- yes when EVERY time we observe something and X is ALWAYS the cause-> well you know, science and predictions.

    Minlay:
    How many of those IC objects whose causes were discovered were biological organisms?

    Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology.

    Minlay:
    How many of the intelligent agents were non-human?

    There are many non-human intelligent designers here on Earth. You would have known that had you ever visted with nature.

    Minlay:
    What evidence do you have that an intelligent designer even existed 500 million years ago?

    I don’t have a time-table. Nor do I need one.

    Minlay:
    All your design cases were caused by humans.

    Nope. And then we have SETI…

    Minlay:
    “Couple that knowledge with the fact we have NEVER observed unintelligent, blind/ undirected (non-goal oriented) processes bringing forth IC or CSI.”

    Minlay:
    But there is no logical barrier to the evolution of IC systems, and we have a ton of evidence to suggest that IC systems can and do evolve.

    Again that they can “evolve” is NOT being debated. They very well could have “evolved” by DESIGN! Read the article “Evolving Inventions” 2003 SciAm.

    The logical barrier to the blind watchmaker is obvious- such processes have NEVER been demonstrated to do anything except alter already existing designs. The instructions for most IC structures are even more IC than the structure itself. AND the structure needs command-n-control and communication links for that. A bac flag is useless without it.

    Minlay:
    We certainly have more evidence of that than IDists have that a designer existed back then.

    If you did we wouldn’t be having this discussion. You can puff out your chest all you want but that will get painful after a while.

    Dr Behe proposed an experiment that would refute an ID icon AND substantiate the claims of anti-IDists. Yet no one, I repeat NO ONE from the anti-ID is going to touch it, even though such an experiment should have been started decades ago.

    Some come on, give it a try:

    Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?

  66. Nick Matzke wrote:

    DaveScot writes,

    “By their silence, the NDE defenders have admitted there were no tests performed to discriminate between chance and design.”

    No design model has been offered for the origin of VDJ recombination, despite my requesting this. Behe couldn’t do it when asked at trial, and you guys can’t do it here.

    Sal still doesn’t get that the whole point of the immune system literature stack at trial was specifically to show that Behe’s version of “detailed and testable” was ridiculous and unreasonable, and that he was only maintaining his claims about IC by waving away massive amounts of evidence with his unreasonable criterion.

    You have to chose, Sal. Shall we require all science to provide near-infinite detail before any model is accepted? (Like Behe requires for evolution) Or, instead of omniscience, shall we go with the standard science has successfully used for hundreds of years, namely, testable models and passed tests?

    Which one is the reasonable standard, Sal?

    Nick, you might have the two of us confused. I’m not DaveScot. :-)

    Take a deep breath, and you’ll be able to reset your registers upstairs.

    Sal
    PS
    By the way DaveScot, it’s good to see you.

  67. Transposition is a form of random muation? How was that figured out?

    Um…by studying transposons and transposition. The vast majority of transposon activity isn’t doing much besides reproducing transposons. 3% of the human genome is DNA transposons and fossils of DNA transposons (much of the rest of the genome is other repetitive elements) and doesn’t appear to be doing much besides propagating itself.

  68. Nick, you might have the two of us confused. I’m not DaveScot. :-)

    I know, I was addressing two different people in one post. First DaveScot, then you.

    Take a deep breath, and you’ll be able to reset your registers upstairs.

    I’m not the confused one. Feel free to answer my question, if you can.

  69. The detail Behe has asked for has been discussed, and is indeed finite. It is the kind of detail that is required by any other science making claims of a mechanism’s ability to create a result – step by step testable models or experiments showing that the claims are actually being demonstrated, including relevant variables. This is surely not too much to ask of a science whose claims are to be taken as ‘fact’, which are as well-attested to as gravity, and which are as proven as the claim that the Earth revolves around the sun.

    For the origin of VDJ recombination, evolutionary biologists have the major steps, they have tested them, and they have convincing and widely accepted model for how VDJ recombination evolved by natural processes.*

    But if hundreds of published research papers are clearly “not enough” for you guys and for Behe (and you are agreeing that the lawyer’s characterization was exactly correct), and you still think you get to say cavalierly that there are “no answers” (even though UD folks apparently now accept the transposon answer after we evolutionists taught them about it on these threads!).

    You demand yet more detail, that every single mutation be reconstructed, even though the main mutations (transposition and rearrangements) account for the major features, and point mutations etc. are uncontroversial “microevolutionary” processes. You also demand that every single ecological interaction, population change, etc. be reconstructed for 500 million years ago, so that you can exactly characterize every selection pressure, even though there is a large amount of work (by Cohn, Gould, and others) showing why natural selection regularly favors receptor diversity.

    This kind of reconstruction is impossible without a time machine, and probably impossible *with* a time machine (i.e. sequencing the genome of every individual fish that lived between 500 and 450 million years ago). And yet this is what you are demanding.

    If this standard of “totally complete knowledge” were required in any other science it would kill it. Take the study of flagellum structure. We know that proteins are exported through the based of the flagellum. This is basically 100% certain. However, we know almost nothing about exactly how this protein export occurs. We know that an ATPase is involved and that it interacts with some other proteins — but we don’t know their structure, how exactly they interact, etc.

    On your logic, no matter much evidence supported the hypothesis of export-through-the base, we couldn’t conclude that proteins are exported through the base of the flagellum, until we knew exactly and completely how it happened.

    Basically, you and Behe are providing an *excuse* for not admitting Behe was wrong when he said scientists had “no answers.” We let Behe make his excuse in Court, and the judge accurately recounted the excuse in his opinion. The judge clearly described Behe’s opinion that the 58 articles were not detailed enough for him. The judge simply realized, along with everyone accept diehard ID fans, that Behe’s infinite-detail criterion was ridiculous.

    You can keep deluding yourselves all you like, but it just means you will make fools of yourselves again and again against informed opposition. But by all means, keep dreaming that you could save the ID case with legal technicalities and by dismissing piles of scientific evidence by employing absurd and tenditious standards. It will just make it easier for us next time in court.

    Later, Nick

    (* Regarding the demand to prove it was “unintentional”, this cannot be done because the hypothesis that a supernatural ID agent miraculously intervened in unspecified ways via mysterious mechanisms cannot be tested or falsified. Hypotheses of mysterious supernatural designer intervention are unconstrained and puts no constraints on the data, and therefore no expectations to be tested. All we can say is that the model using specific natural processes has been highly successful when put to experimental test.)

  70. Matt: “What evidence do you have that an intelligent designer even existed 500 million years ago?”

    Joseph: “I don’t have a time-table. Nor do I need one.”

    I see, so you don’t feel that it’s necessary to demonstrate the actual EXISTENCE of the one doing the designing, or provide any evidence for it whatsoever. This is not how science proceeds.

    “Gee I guess I stand refuted. LoL! But anyway- yes when EVERY time we observe something and X is ALWAYS the cause-> well you know, science and predictions.”

    And EVERY time that designer is human. Please give me an example of an intelligently designed IC object that was designed by a non-human designer. I’ll give you some starters. Is a spider web intelligently designed? How about a beaver’s dam? A bee hive? How about the tiny magnetite crystals that magnetic bacteria can form? This is something I’ve always wanted to know, but never got a straight answer from the ID crowd.

    So what predictions can be made from the logical argument you just gave? Can any of these predictions be verified by ID researchers?

    “Again that they can “evolve” is NOT being debated. They very well could have “evolved” by DESIGN! Read the article “Evolving Inventions” 2003 SciAm.”

    Are you really sure that the ability of evolution is not being debated? I have no problem granting the argument that evolution could have been designed, but again, there will have to be evidence for it.

    “The logical barrier to the blind watchmaker is obvious- such processes have NEVER been demonstrated to do anything except alter already existing designs.”

    That isn’t a logical barrier, that’s an empirical one. We can easily form hypothetical models for how an IC system could have evolved. If you want I can give you several simple examples. There are also numerous examples of biological processes that have created novel functions. The ironic thing is that the immune system creates a novel function everytime it is activated by an infection. I don’t think you want to argue that the immune system itself is an intelligent agent. I can give you other examples if you’re interested.

    Me: “We certainly have more evidence of that than IDists have that a designer existed back then.”

    Joseph: “If you did we wouldn’t be having this discussion. You can puff out your chest all you want but that will get painful after a while.”

    Really? Because this whole discussion began with the presentation of 58 articles on the evolution of the immune system. Where are the 59 papers on the existence of an IDer?

  71. You have to chose, Sal. Shall we require all science to provide near-infinite detail before any model is accepted? (Like Behe requires for evolution)

    That’s a leading question with respect to Behe requiring infinite detail. Thus you question is disqualified.

    I already described what you guys could consider providing just based on basic population thoery in the absence of hard evidence. If it turns out you need unrealistic populaiton resources to achieve your ends, then you might realize your theory is DOA.

    Or, instead of omniscience, shall we go with the standard science has successfully used for hundreds of years, namely, testable models and passed tests?

    We should go with testable models, but so far the only tests passed are suggestions of similarity. Big deal. It does not settle the issue of what mechanisms were in play for the various reasons I pointed out. You repeat again the equivocation between Darwinism and evolution. The two are not equal.

    Science should welcome increasing scrutiny of its theories, because its in the presence of anomalies that interesting things are discovered. Behe suspects that Darwinism cannot account for the majority of molecular evolution, and that is highly consistent with initial findings of population genetics. Brian Goodwin, Salthe, others make a good case Darwinism as the mechanism is a bit pre-mature.

    Which one is the reasonable standard, Sal?

    More leading questions. But as far as good standards, how about the standards which established real scientific theories like:

    1. universal gravitation
    2. atomic theory of chemistry
    3. electro-magnetism
    4. thermodynamics
    5. celestial mechanics

    All by design-friendly scientists.

  72. Nick Matzke,

    I have to add, I think we do not serve the cause of science well if we give the impression forensic speculation like evolution should receive the same level of acceptance as operational theories like electromagnetism.

    Thus, if you want lower standards of acceptance for forensic theories, you should make it clear that forensic theories have far lower threshhold of acceptable proof in your eyes. In other words, you should communicate to your audiences that to get evolution to be accepted requires lowered standards of proof.

    Salvador

  73. NickM

    Is it your position that the evolution of the immune system was driven by chance mutations filtered by natural selection? If so, what tests were performed to verify or falsify the assertion that the mutations were generated by chance?

  74. Maybe this will help Nick et al understand the issues.

    A fertilized human egg cell doesn’t have an immune system. The immune system begins to develop during the embryo stage and is fully developed in the fetal stage. There is nothing left to chance in this process. The egg cell contains all the information and mechanisms needed to eventually build a functional, mature immune system. Ontogeny proves that single cells can have a preprogrammed plan of diversification into many different cell types and complex organization. Nothing in the normal course of ontogenesis is due to chance. This is the design model I hold.

    Now I ask again, in the phylogenetic evolution of the immune system, what tests were performed to discriminate between a preprogrammed sequence of events leading to an immune system and a random sequence of events leading to an immune system?

    If you can’t point to any tests that can and did discriminate between programmed and random evolution of the immune system what justification do you have in saying it was due to chance instead of design?

  75. Now I ask again, in the phylogenetic evolution of the immune system, what tests were performed to discriminate between a preprogrammed sequence of events leading to an immune system and a random sequence of events leading to an immune system?

    And that really is the central question, isn’t it.

  76. Transposition is a form of random muation? How was that figured out?

    NickM:
    Um…by studying transposons and transposition. The vast majority of transposon activity isn’t doing much besides reproducing transposons. 3% of the human genome is DNA transposons and fossils of DNA transposons (much of the rest of the genome is other repetitive elements) and doesn’t appear to be doing much besides propagating itself.

    As far as we know transposition of genetic elements are as random as statements in C++ programs. For example someone who didn’t understand C++ would think that “go to” “if else”, etc. were random events. C++ programmers know better.

    Again evolutionists rely on our ignorance in order to declare that which is not understood as being random.

    NickM:
    Regarding the demand to prove it was “unintentional”, this cannot be done because the hypothesis that a supernatural ID agent miraculously intervened in unspecified ways via mysterious mechanisms cannot be tested or falsified.

    But ID does NOT say anything about a supernatural ID agent. That is because even that anti-ID position “turtles down” to something beyond nature. Also design is a mechanism.
    ID can be tested by the concepts of IC and/ of CSI. Either they exist or they do not. All of our experience demonstrates that both only arise via intelligent agencies. Therefore if it is demonstrated, for example, that life can arise from non-living matter via unintelligent, blind/ undirected (non-goal oriented) processes ID would be falsified.

    NickM:
    Hypotheses of mysterious supernatural designer intervention are unconstrained and puts no constraints on the data, and therefore no expectations to be tested. All we can say is that the model using specific natural processes has been highly successful when put to experimental test.

    Way to go Nick! You just proved you can create a strawman and attempt to knock it down! BTW both intelligence AND design are natural processes. And there isn’t anything “specific” about RM culled by NS.

    ——————————————————————————

    Joseph: “I don’t have a time-table. Nor do I need one.”

    Minlay:
    I see, so you don’t feel that it’s necessary to demonstrate the actual EXISTENCE of the one doing the designing, or provide any evidence for it whatsoever. This is not how science proceeds.

    Nice goal post move. No one said the designer has to still exist. The data we do have says at least one did exist but that data did not come with a time stamp.

    “Gee I guess I stand refuted. LoL! But anyway- yes when EVERY time we observe something and X is ALWAYS the cause-> well you know, science and predictions.”

    Minlay:
    And EVERY time that designer is human.

    Wrong. But even if it were true- so what? All we need is the knowledge of what intelligent agencies can do and contrast that knowledge with the knowledge of wjay nature, acting freely, can and cannot do.

    “Again that they can “evolve” is NOT being debated. They very well could have “evolved” by DESIGN! Read the article “Evolving Inventions” 2003 SciAm.”

    Minlay:
    Are you really sure that the ability of evolution is not being debated?

    Ability of evolution? What is that? The debate is about the ability of mechanisms.

    Minlay:
    I have no problem granting the argument that evolution could have been designed, but again, there will have to be evidence for it.

    There isn’t any evidence for the anti-ID position so why do you grant it a free pass?

    “The logical barrier to the blind watchmaker is obvious- such processes have NEVER been demonstrated to do anything except alter already existing designs.”

    Minlay:
    That isn’t a logical barrier, that’s an empirical one.

    Actually it’s both.

    Minlay:
    We can easily form hypothetical models for how an IC system could have evolved.

    Not without breaking many rules.

    Minlay:
    Really? Because this whole discussion began with the presentation of 58 articles on the evolution of the immune system.

    And AGAIN- Not one of those 58 discuss blind watchmaker-type processes! What part of that don’t you understand?

    And if that antic happens again the anti-IDists will be eating crow. Of that I am very sure.

    BTW beaver dams and lodges are intelligently designed. Nature, operating freely, could not have produced either.

  77. I take it neither NickM or Minlay will even attempt to answer the following:

    Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?

    Typical but still sad…

  78. 54: Joseph asks: “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?”

    Ofro’s response: “The reason is that the mutations can not only affect a protein’s function but also its expression level. [plus detailed explanation how]“

    Joseph’s new response: “But the function is not affected.“

    You are asking me how there can be a mutation that does not affect functionality, I give you an example, and then you turn 180 degrees and challenge my answer by saying that function is not affected. Sorry, I am at a loss about what you want.

  79. 76. Joseph: “Transposition is a form of random muation? How was that figured out?”

    First, I think there are very few people who would disagree with classifying any change of DNA sequence as a mutation. Second: why random? Because at least in the test tube, transposons behave randomly; there are even commercial kits available that use transposons to deliberately and randomly shift DNA around, such as for the purpose of sequencing long stretches of DNA. see http://www.neb.com/nebecomm/pr.....tE7100.asp

    So if you are challenging the notion that this enzyme system does not have at least a random component in its action, wouldn’t this be something worthwhile for the molecular biologists among the ID crowd to disprove experimentally?

  80. 54: Joseph : “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?”

    snip

    Joseph” It does if we were discussing variations within a population. However we both know we aren’t discussing that.”

    I guess it boils down to your denial that if a species accumulates many mutations over a long time, resulting in changes of morphology as well as inner workings (such as in the nervous system, but could be other organs, too), that this process could result in a related species. I am not asking for turning a fish into a quadruped. I am only asking about mouse vs. rat or wolf vs. dog. Is there not even the theoretical possibility of that?

  81. Joseph said:
    “Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?”

    Is someone acually claiming that our human immune system evolved from the lamprey’s immune system? My goodness! Anyway, I have a question: if there is an intelligent designer at work, why do we even need an intelligently designed immune system to protect us from intelligently designed pathogens? What kind of purpose and morality is inferred from a designer who creates life forms, only to turn around and design parasites, etc. to sicken, torture and kill them? (For this example I’m assuming there is but one designer.)

  82. Karen,
    You are conflating religion and philosophy with design detection.
    Inferring design is not inferring moral purpose.

    If you are concerned rather with the problem of evil as pertains to the God of Christian belief then Bill Dembski’s theodicy might be for you.
    http://www.designinference.com/

  83. ofro

    Just about anything is possible. It’s possible that tiny invisible pixies from Mars are the mechanism responsible for organic evolution. Science is all about narrowing down the list of the possible to a list of the probable. So again I point to the programmed development of the immune system during ontogenesis and ask what tests were performed to rule out the same programmed process occuring during phylogenesis. I’m of the opinion that they are basically the same diversification process at different scales – neither is or was a matter of chance.

  84. DaveScot,
    ” …and ask what tests were performed to rule out the same programmed process occuring during phylogenesis”

    I am not an immunology expert and may not be the ideal person to ask, but from what I understand from the field and from your question, I think I can exclude your proposed scheme just by referring to the textbooks (I don’t have any in front of me right now to verify what I am writing). The development of the immune system in the embryo, like so much else in the embryo, follows a fairly specific program that is set up by (what I understand, but again, I am not the expert here) a sequential activation of hox genes, followed by activation of increasingly “lower-level” systems and transcription factors with more specific locational specificity. (Of course there are also many transcription factors that are not location- or tissue-specific).

    During reproduction, which obviously must happen if you want to progress through any evolutionary pathway, these mechanism play no role, and totally different regulatory pathways are in charge. If hox genes, and all the other pathways that set up the immune system, were involved, this would have been detected even without specifically looking for that. So your proposal of the “same programmed process occuring during phylogenesis” does not work.

    Perhaps your statement was a bit more general in that some other program exists (or existed) according to which the immune system had no choice but developing during the evolutionary process over many generations. I am not sure how to answer that. I think you are asking for a test of whether some (any?) not-yet-specified programmed process exists which determines the generation of an immune system that had not occurred in previous generations. (Is that a version of genetic front-loading that permits future diversification into many different species?).

    I can only come up with two possible replies:
    1. Considering the amount of work that has been put into learning about the immune system and its possible evolutionary precursors, I would be very surprised that some regulatory pathway should have been overlooked. No matter how biased you may consider scientists to be against directed evolution, if you want to put a negative spin on scientists, you will also accept that a) if a scientist discovers a potentially revolutionary mechanism, he/she will make sure that everybody knows about it, either through the scientific literature or by trumpeting it in the popular press; and b) that there will be a horde of other scientist jumping on it to test and hopefully disprove it. (I am exaggerating a bit, but the essence is there; and this is how the bad stuff eventually is weeded out). In addition, negative results, i.e. the fact that one couldn’t find something one was looking for, are much less likely to be published. Overall, no such proclamation of a regulatory principle or program has ever been made in my knowledge. So my tentative conclusion is that your question may already have been answered, unnoticed by anybody.

    2. (I don’t want to sound too antagonistic, so please excuse if I come across as too strong for you) If a proof is required, it is always better to demonstrate the existence of a process/object than to demonstrate its absence. You are essentially asking your scientific opponent to demonstrate the _absence_ of something that you propose as an (competitive) alternative. I would invite scientists on the ID side to put efforts into demonstrating the _presence_ of what you postulate.

  85. 54: Joseph : “So how can changes that do NOT affect functionality at the molecular level produce profound effects at the morphological level?”

    snip

    Joseph” It does if we were discussing variations within a population. However we both know we aren’t discussing that.”

    Ofro:
    I guess it boils down to your denial that if a species accumulates many mutations over a long time, resulting in changes of morphology as well as inner workings (such as in the nervous system, but could be other organs, too), that this process could result in a related species.

    Can’t deny what has never been demonstrated. Then there is the following to consider:

    Extrapolating From Small Changes:

    If one desires to extrapolate small changes into large changes by simply adding time, one requires independent evidence to justify this move. The problem is that we really don’t know how evolution occurs. And when talking about the evolution of the mammalian middle ear bones, we should not forget that we are still basically in the dark in trying to explain how both a mammalian and reptilian zygote actually develops the middle ear and jaw bones, respectively. Without this knowledge, attempts to explain such a transition as a function of a series of small, incremental changes stretched across time are rooted in ignorance. That is, we don’t truly understand neither the process of development nor the process of evolution and without such knowledge, there is no reason to think we are on safe ground when employing (1).

    Ofro:
    I am not asking for turning a fish into a quadruped. I am only asking about mouse vs. rat or wolf vs. dog. Is there not even the theoretical possibility of that?

    Wolf/ dog is more of the variations I was talking about.

    Joseph: “Transposition is a form of random muation? How was that figured out?”

    Ofro:
    First, I think there are very few people who would disagree with classifying any change of DNA sequence as a mutation.

    That is irrelevant.

    Ofro:
    Second: why random? Because at least in the test tube, transposons behave randomly; there are even commercial kits available that use transposons to deliberately and randomly shift DNA around, such as for the purpose of sequencing long stretches of DNA.

    Again they are random only due to our ignorance. This approach is like trying to figure out the output of a C++ programm by only looking at the ASCII representation of the output.

    Ofro:
    So if you are challenging the notion that this enzyme system does not have at least a random component in its action, wouldn’t this be something worthwhile for the molecular biologists among the ID crowd to disprove experimentally?

    Once again-

    Dr. Spetner discussing transposons:
    The motion of these genetic elements to produce the above mutations has been found to a complex process and we probably haven’t yet discovered all the complexity. But because no one knows why they occur, many geneticists have assumed they occur only by chance. I find it hard to believe that a process as precise and well controlled as the transposition of genetic elements happens only by chance. Some scientists tend to call a mechanism [I]random[/I] before we learn what it really does. If the source of the variation for evolution were point mutations, we could say the variation is random. But if the source of the variation is the complex process of transposition, then there is no justification for saying that evolution is based on random events.”

    —————————————————————————————

    Karen asks:
    Anyway, I have a question: if there is an intelligent designer at work, why do we even need an intelligently designed immune system to protect us from intelligently designed pathogens?

    No one said the design had to be “perfect” or that even if it started out “perfect” that it had to remain that way.

    Karen:
    What kind of purpose and morality is inferred from a designer who creates life forms, only to turn around and design parasites, etc. to sicken, torture and kill them?

    Tell us Karen, what do you know about ID? What would happen on an Earth in which humans did not die? People die and we find out why. It’s a discovery process. And that fits in nicely with the premise of “The Privileged Planet”.

  86. 85: Joseph quoting from Extrapolating From Small Changes:
    “And when talking about the evolution of the mammalian middle ear bones, we should not forget that we are still basically in the dark in trying to explain how both a mammalian and reptilian zygote actually develops the middle ear and jaw bones, respectively. Without this knowledge, attempts to explain such a transition as a function of a series of small, incremental changes stretched across time are rooted in ignorance.”

    I glad to see that the notion of a “gap” in the fossil record has been abandoned here. Time to move the bar.

    Also:
    Ofro: “Second: why random? Because at least in the test tube, transposons behave randomly; there are even commercial kits available that use transposons to deliberately and randomly shift DNA around, such as for the purpose of sequencing long stretches of DNA.”

    Joseph replie: “Again they are random only due to our ignorance. This approach is like trying to figure out the output of a C++ programm by only looking at the ASCII representation of the output.”

    I don’t know where the “ignorance” is to be found. I have the DNA sequence in my laboratory notebooks and know where the transposon insertions are. That is an experimental observation not an assertion from ignorance. I am not claiming that I know the exact biochemical/enzymatic mechanism of the process (is that what you mean by your C++ code?). I know the experimental outcome, and that is what I have claimed.

  87. In comment #65 by Joseph:

    “Minlay:
    How many of those IC objects whose causes were discovered were biological organisms?

    Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology.”

    I just wanted to point out a misconception by Joseph here. The method for detecting genetically modified foods is not based on the ID methodology of probabilities. What it’s based on is knowing _in advance_ what the genetically modified string of genetic code looks like and _then_ searching for it. Obviously, unless we know ahead of time what the “intelligent designer” was capable of, this tried-n-true detection methodology does nothing in detecting design in non(human)-modified biological organisms.

  88. Sorry, I’ve been busy at work so I haven’t had much time to continue this conversation.

    Joseph: “Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology.”

    To add to Monimonika’s point, with regards to forensics, archaeology, and GM foods, in all those cases, any inference to design takes into account knowledge of the designer, i.e. humans. Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old. No forensic scientist is going to propose that a person was murdered using technology that doesn’t exist. All design inferences in these fields were made by forming a model of how a designer created the object, then looking for evidence to support that model. For example, an archaeologist might examine an arrowhead-shaped rock for evidence of chipping, of a type of technique he/she knows that tribes (that existed at the time the arrowhead was created) commonly used.

    With ID, no information about the capabilities, motives, or existence of the designer is even looked for, and therefore no models for how the designer may have created the supposed designs are made. Without a model, there’s nothing to look for, and therefore there’s no science.

    (I’ll try and address these other points when I have time)

  89. “Minlay:
    How many of those IC objects whose causes were discovered were biological organisms?

    Me:
    Tell us Minlay, what prevents tried-n-true design detection methodology from being used on biological organisms? And yes we can discover genetically modified foods via ID methodology.”

    Moni:
    I just wanted to point out a misconception by Joseph here. The method for detecting genetically modified foods is not based on the ID methodology of probabilities.

    Probabilities is NOT the ONLY ID methodology. Had you known about ID you would have known that.

    Minlay:
    To add to Monimonika’s point, with regards to forensics, archaeology, and GM foods, in all those cases, any inference to design takes into account knowledge of the designer, i.e. humans.

    Irrelevant.

    Minlay:
    Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old.

    Then they have a problem. A major problem.

    Minlay:
    With ID, no information about the capabilities, motives, or existence of the designer is even looked for, and therefore no models for how the designer may have created the supposed designs are made.

    Again if we knew the capabilities of the designer we would NOT have a design inference- design would be a given. also- the ONLY way to make ANY determination about the designer in the absence of direct observation or designer input is by studying the design in question THAT is a fact of life. Also the design inference makes both the designer and the process separate questions- just as Wm. DEmbski explains in “No Free Lunch”.

    Minlay:
    Without a model, there’s nothing to look for, and therefore there’s no science.

    We look for CSI and/ or IC. OR we could start with Behe’s simple criteria:

    “Our ability to be confident of the design of the cilium or intracellular transport rests on the same principles to be confident of the design of anything: the ordering of separate components to achieve an identifiable function that depends sharply on the components.

  90. And while we are waiting:

    Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?

  91. Comment #89 by Joseph:

    “Moni:
    I just wanted to point out a misconception by Joseph here. The method for detecting genetically modified foods is not based on the ID methodology of probabilities.

    Probabilities is NOT the ONLY ID methodology. Had you known about ID you would have known that. ”

    I apologize for my ignorance, but only if you can please explain this other part(s) of the ID methodology (of detecting intelligent design) that relates to the methodology of detecting genetically modified foods. As said before, detecting GM foods depends upon knowing the sequence of the modified part of the genetic code before going out to look for it.

    You most likely will not make this particular arguement, but I just want to specify that I will not accept analogies of “parts of biological organisms” to “parts of man-made, non-biological, machinery”. Reasons on why I dismiss this analogy approach are: 1) it assumes human intelligence when making distinctions, not necessarily that of a non-human designer, and 2) man-made, non-biological, machinery are built from parts assembled by other beings (humans in this case) rather than being reproduced from each other (plus, they don’t grow). Again, I don’t believe that you will make this arguement, but I didn’t want to read about it from others.

    Joseph, please tell me what I am missing since I admit that I haven’t been following the ID methodology too closely and most likely missed something due to the biased reading of the subject that I encountered early on.

    Thank you,

    Monimonika

  92. Oh, and one more thing. I have to call on an error by Minlay in comment #88:

    “Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old. … For example, an archaeologist might examine an arrowhead-shaped rock for evidence of chipping, of a type of technique he/she knows that tribes (that existed at the time the arrowhead was created) commonly used.”

    I have to side with Joseph on this one. If an archaeologist found an arrowhead-shaped rock with evidence of chipping/modifications in sediment that’s 10 million years old, then the finding would be picked up and studied like crazy, with multiple theories (here, “theory” means guesses) on how it came to be the way it is. It wouldn’t be tossed aside. Of course, there would be more digging for other clues and arrowhead-shaped rocks, which would take time and would, hopefully, lead to a better and better set of explanations (which, depending on the evidence, may also include “sheer coincidence” as a possiblity).

    Just one arrowhead-shaped rock (with evidence of modifications) would not be enough to solidly claim anything, of course. The main point is that, it will all depend on what we can conclude from the evidence surrounding the may-be arrowhead-rock. It could be a coincidence. It could be that there existed a tool-making creature prior humans (evidence of which should turn up in other forms

  93. Me: “Clearly no archaeologist is going to propose that a rock shaped like an arrowhead was intelligently designed, if the arrowhead was found in a sediment that’s 10 million years old. … For example, an archaeologist might examine an arrowhead-shaped rock for evidence of chipping, of a type of technique he/she knows that tribes (that existed at the time the arrowhead was created) commonly used.”

    Sorry for the sloppy wording, I wasn’t trying to imply in the first sentence that the arrowhead-shaped rock had evidence of chipping, just that it was SHAPED like an arrowhead, nothing more. I’m not sure if any evidence of manufacturing would be left on a 10 million year old piece of rock. However, in monimonika’s scenario: “It could be that there existed a tool-making creature prior humans”, the study of this model would proceed by a) looking for evidence that such a creature existed, b) hypothesizing what method the creature used to create the arrowhead and looking for other objects that contain similar manipulations, c) hypothesizing what the function of the arrowhead-shaped rock was (somehow I doubt that creatures 10 million years ago hunted with bow and arrow), and looking for objects that may complement such a function. Essentially what I’m describing is a series of testable models to explain the origin of that arrowhead. I still think it’s highly unlikely that anyone would think a 10 million year old rock was intelligently designed just because it bore the shape of an arrowhead, but if they found real evidence of manipulation, that’s how I think they might proceed.

    Do you see IDists trying to develop testable models to explain the origins of IC biological systems? No, and the reason is that it would require some hypotheses about the nature and capabilities of the designer.

  94. Joseph, I’m trying to avoid the point-by-point response technique, because it only takes a few exchanges from each of us before our posts become unreadible. If there are points you really want me to address that I didn’t, please reiterate them. As for the lamprey question, I just haven’t gotten around to it, but I don’t like feeeling like I’m being coerced to answer any particular question (see DaveScot), so I usually tend to ignore them.

    Joseph’s questoin: “Just how can one test or falsify the premise that the human immune system “evolved” from the lamprey’s via unintelligent, blind/ undirected (non-goal oriented) processes?”

    The lamprey’s immune system may not be the best system to use for this example, because about 2 years ago, we discovered evidence that they have their own version of the adaptive immune system that’s quite different than ours. I don’t know how long ago we diverged from the extant lamprey, but let’s say 500 million years ago. That’s a lot of time for them to evolve their own system. So I’m just going to use a generic jawless vertebrate that existed after the lamprey/jawed vertebrate split.

    Since you’re not going to argue the details of how we think the immune system evolved, I’ll just focus on the “unintelligent, blind/undirected (non-goal oriented) process. However, here’s the basic model that I’ll be working with. In a jawless vertebrate, a transposon containing the RAG-1 and RAG-2 genes, and flanked by recombination signal sequences (RSSs), integrated into an antigen receptor gene, near the point on the gene that encodes the antigen binding pocket. During the development of the lymphocytes that express this gene, as the gene becomes transcriptionally active, so does the RAGs, which then undergo a second transposition reaction, removing the transposon, and leaving the gene slightly different than when it entered. This only happens in a subset of lymphocytes (because of the randomness of the transposition reaction), but in every lymphocyte it happens to, it leaves the antigen receptor gene slightly different, creating a diversity of antigen receptor genes, and increases the types of antigens that these genes can bind. As the population of jawless vertebrates is exposed to pathogens in their environment, the one animal bearing this unique antigen receptor has a competitive advantage, being able to fight off infections from a broader range of pathogens. Eventually it’s offspring take over the population, and a new system emerges.

    That’s the basic model. Each sentence in that description I can back up using evidence from the 58 papers originally referenced. Now your issue seemed to be not that this sequence of events occured, but rather whether or not it could be accounted for by the evolutionary mechanisms mainstream scientists recognize. To that end, there are certain predictions that a system of random mutation and natural selection makes. One is that genes will continuously mutate, and the mutations in essential regions of genes will likely be detrimental (though not always!), whereas mutations in non-essential, or non-coding regions will be effectively neutral. So if we compare sequences of organisms within those genes, the prediction is that coding regions will have fewer differences than non-coding regions, and essential coding-regions will have fewer differences than non-essential regions. There’s also the issue of silent mutations, which don’t affect the protein sequences, and non-synonymous mutations, which do. In addition, there is the issue of time. Organisms which diverged from humans longer ago will have more differences in their genetic sequence than organisms which diverged more recently. Taken together, what this means is that there’s a range of possible sequences that we expect to find in any given lamprey gene. Since this is a probablistic argument, we expect that if examine ALL the lamprey genes and compare them to their homologues in humans, we will find a bell curve, with some genes being more similar (just due to probability), and some genes being more dissimilar. The mean value or peak of that curve will have a percent similarity to humans that’s inversely proportional to the predicted age (based on fossil records and cladistics) that the organism diverged from humans. In other words, the further ago the two organisms diverged, the smaller their average percent similarity of homologous genes will be. A potential falsifier of “Darwinian” evolution is if the average percent similarity of homologous genes for lamprey vs. human is greater than that for mouse vs. humans. Also, I should point out that because lamprey diverged from humans at the same time it diverged from mice, we also predict that the percent similarity of lamprey vs. humans will be the same as lamprey vs. mice (or lamprey vs. any jawed vertebrate). The same idea applies to every other genome we have sequenced, and so a phylogeny can be made of all the genomes sequenced, and “Darwinian” evolution predicts that these phylogenies should match the phylogenies we’ve made using traditional methods (fossils records, cladistics). I would guess that these phylogenies don’t match 100% of the time, and I would argue that in those cases the fossil record is wrong, and so another prediction of “Darwinian” evolution is that in cases where they don’t match, the fossil record will be found to be in error. It is a necessary condition of common descent that all organisms are contained within one “true” phylogeny, though we don’t necessarily know exactly 100% what that phylogeny is. Note that for those who do not believe in common descent, there is absolutely no requirement for anything to fit in a phylogeny.

    So to answer your question, we can test whether or not the model of how the human immune system evolved from lamprey or better yet tunicate immune systems by analyzing the sequence data and seeing if it falls within our predicted ranges. It should also be noted that intelligent design makes NO sequence predictions, and therefore all sequences are equally likely.

    Here are some other ways to test the model. We should be able to generate a pathway for each of the major steps in the evolution of the immune system (after the initial transposon insertion I described above). There are a number of features that we must take into account. In humans, there are actually 7 genes that can undergo V(D)J recombination: TCRalpha, TCRbeta, TCRgamma, TCRdelta, and Igkappa, Iglambda, and IgH (heavy chain). If “Darwinian” evolution is true, than all of these genes should have evolved from a single antigen receptor, and therefore all 7 should be able to fit a phylogeny. Furthermore, a phylogeny should be possible for EVERY organism that has a V(D)J recombination system. For example, while mice are similar to humans, there are some key differences in their genomic organization. Furthermore, all sharks, fish, birds, and reptiles should also each fit into their own individual phylogeny, and the phylogenies of each should match (to the extent that their systems are similar). For example, if mammals and birds both contain Igkappa and Iglambda genes (which they do), then their common ancestor (reptiles) at one point contained both Igkappa and Iglambda genes. Since the Igkappa and Iglambda genes are quite similar to each other, then the prediction is they were once a single gene in one of our ancestors. The timing of their divergence (via gene duplication) should match between birds and mammals, and their split should be consistent with all the other phylogenies. So if there is only a single Igkappa/Iglambda gene in reptiles, then there should not be a distinct Igkappa or Iglambda gene in any of the predecessors of reptiles (amphibians, fish, sharks). My basic point is that there are a LOT of rules to make the phylogenies consistent with each other. However, a lot of what I described applies to the notion of common descent, not necessarily “Darwinian” evolution, but the sequence data is very Darwinism-specific. That the two are highly interwoven is a consquence of our current evolutionary theory.

    There have been a few roadblocks discovered along the way. One example is that intially there were thought to be two random insertions of the RAG transposon into an antigen receptor gene. One split the gene into V and J segments, and a second one split it again into V, D, and J. Because some genes have only V and J, while others have V, D, and J, if all of these genes evolved from a single gene then there had to have been two transposon insertions, at totally different times. This wasn’t a very feasible model. However, later on we discovered that an errant recombination reaction could actually create a novel gene segment, which would explain how a D segment was created through non-intelligent means and without appealling to another transposition reaction. Here’s a second example. Not all recombination signal sequences are the same. Some have a 12 base pair gap, and others have a 23 base pair gap. Only RSSs with a 12 bp gap can rearrange with RSSs with a 23 bp gap (this is called the 12/23 rule). In some genes, the V segments have a 12 bp gap, and in other genes the Vs have a 23 bp gap. This is totally inconsistent with common descent via “Darwinian” evolution, but of course it would be easy for an IDer to flip the RSSs. However, a few years later, it was discovered that another type of errant recombination could flip the RSSs. Again, a major problem for the evolution of this system (via “Darwinian” evolution) was solved. So here is another prediction of “Darwinian” evolution. For every situation that would appear to falsify the proposed pathway, a novel mechanism will be found to explain it. It’s happened twice so far.

    So what I’ve presented here (which was contained within the 58 references all along!) is a model for how the adaptive immune system could have evolved. The model is detailed (it could easily fill a book, just for the adaptive part), and testable (as I have shown above). And a major point in its favor is that there are researchers out there that are actively testing it. It’s one thing to propose an experiment, and another thing entirely to conduct one. Where is the actual ID research on the origin of any IC system? So here we have a situation where the pro-evolution side is actively studying the origin of this system via evolution using the scientific method (i.e. developing and testing models), and is achieving real tangible results. And on the ID side, no one is proposing an actual model, no one is conducting research on an ID model for any IC system, and certainly no one has produced any actual results to support ID.

    So let me turn this question back to you: Describe a model for the origin of any IC biological system by intelligent design, and show how this model is testable and/or falsifiable.

  95. To Monimonika,

    Counterflow does very nicely. Counterflow being that which nature could not or would not do if left to operate freely. Therefore if we see an insulin producing sequence in bacteria we would be correct in inferring it was put there by an intelligent agency. That would also apply to GMF. All that would take is to “know” what a plant’s, for example, genome should be and compare that to what we have in front of us (the suspected modified plant).

    ————————————————————————————

    Minlay:
    Do you see IDists trying to develop testable models to explain the origins of IC biological systems?

    Yes, IDists say they originated by design. The process and the designer are separate questions.

    Minlay:
    No, and the reason is that it would require some hypotheses about the nature and capabilities of the designer.

    Reality demonstrates that the ONLY way to make ANY determination about the designer or the process in the absence of direct observation or designer input is by studying the design in question. What part of that don’t you understand?

    For example what could you tell about the Wright Brothers just by studying the jets of today? Could you deduce how they produced their first plane?

    First you detect the design, then you study it. THAT is ID- detection AND understanding.

    Evolutionists insist on making evolution and abiogenesis separate questions even though life’s origins directly impacts its subsequent evolution- if life didn’t arise from non-living matter via unintelligent, blind/ undirected (non-goal oriented) processes there would be no reason to infer its subsequent diversity arose via those types of processes.

    AND we don’t even know if mutations can allow for the range of change required if all of life’s divesity owed its collective common ancestry to some unknown population of single-celled organisms which just happened to have the ability to asexually reproduce.

    BTW thanks for your long response. I will get back to you on that…

    How does one test ID? By the concepts of IC and/ or CSI. How does one falsify ID? By showing that either can arise in the absence of an intelligent agency.

  96. Me: “Do you see IDists trying to develop testable models to explain the origins of IC biological systems?”

    By Joseph: “Yes, IDists say they originated by design. The process and the designer are separate questions.”

    But you haven’t even described the process of design for IC biological systems. All you said was the word ‘design’. What process are you referring to?

    Joseph again: “How does one test ID? By the concepts of IC and/ or CSI.”

    Can you be more specific here? Can you describe an actual experiment that an ID researcher could perform to test whether or not an IC biological system could originate by intelligent design?

    Joseph: “How does one falsify ID? By showing that either can arise in the absence of an intelligent agency.”

    Unfortunately, that would not falsify intelligent design. It’s entirely possible an IDer could have used evolution to create an IC object. Or that the IDer created the object in a way indistinguishable from evolution. Or that evolution could have created the object, but didn’t, and the IDer did. It would make the IC to ID inference worthless, but it wouldn’t falsify ID.

    Incidently, we’ve already shown that IC systems CAN arise in the absence of intelligent agency. Any hypothetical model will do that. What we haven’t shown (in the opinion of the IDists) is that IC systems HAVE arisen in the absence of intelligent agency. Again, this goes back to the logical vs. empirical argument of IC. There is no logical barrier to the evolution of IC objects by “Darwinian” evolution.

  97. minlay: “I see, so you don’t feel that it’s necessary to demonstrate the actual EXISTENCE of the one doing the designing, or provide any evidence for it whatsoever. This is not how science proceeds.”

    Joseph: “Nice goal post move. No one said the designer has to still exist. The data we do have says at least one did exist but that data did not come with a time stamp.”

    I didn’t say the designer had to still exist, just that it had to at one point. I’m assuming the data that you have is the empirical argument we’ve been discussing, meaning you don’t have any independent evidence of the existence of a designer.

    Joseph:“the ONLY way to make ANY determination about the designer in the absence of direct observation or designer input is by studying the design in question. THAT is a fact of life.

    So what determinations have you been able to make regarding the designer based on studying the design?

  98. Sorry about commenting on a semi-old post, but I wanted to get my thoughts straightened out a bit.

    First, a thank you to Joseph for an answer that made me think a bit. If Joseph is still reading this thread (not likely, I know) I’d like to know if the idea of counterflow can be applied to the bacteria that eats nylon.

    Nylon is a material that was obviously designed by humans (since we know the individuals who did so) and can’t be found in nature (barring its introduction by humans). Wouldn’t that seem to make the ability of the nylon-eating bacteria artificial? Was it intelligently designed? How? Was there some other (non-evolutionary) mechanism?

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