Home » Evolutionary biology, Intelligent Design » Another Day, Another Bad Day for Darwinism

Another Day, Another Bad Day for Darwinism

In the latest issue of Nature, a definitive role for pseudogenes is established. In the last sentence of the Abstract the authors conclude:

These findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs.

Haven’t read the full article* (no time at present), but there’s a related link at PhysOrg.com that gives an overview.

Yes, “junk” DNA now “communicates” with itself. A new “language”, an RNA language, is discovered. Another 30,000 pieces of functional information (over and above proteins) are part of cell architecture. And even more for Darwinists to explain per RM+NS. And the old standard explanation, of gene duplication and pseudogenes ‘evolving’ new function, takes a hit. You’ve got to feel bad for these Darwinists. What’s tomorrow going to bring!?!

*BTW, somehow I gained access to the pdf version of the article.

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105 Responses to Another Day, Another Bad Day for Darwinism

  1. PaV:

    Excellent article! And really bad news to the fans of junk DNA.

    The findings presented in this study have allowed us to reach a number of conclusions. First, the discovery of an miRNA decoy function for pseudogenes identifies these transcripts as biologically active units. We show that PTENP1 and KRAS1P affect the levels of their cognate genes and are possibly involved in disease pathogenesis. Thus, the analysis of pseudogene expression level and genomic status in tumorigenesis needs to be undertaken systematically to further our understanding of disease progression.

    And:

    We also demonstrate that pseudogenes such as PTENP1 can derepress their cognate genes, even when expressed at lower levels (Supplementary Fig. 3a and Fig. 2f–h). We propose that pseudogenes are ‘perfect decoys’ for their ancestral genes, because they retain many of the miRNA binding sites and can compete for the binding of many miRNAs at once.

    So, pseudogenes seem to be functional. Who would have said that? (Perhaps, only those silly IDists).

    And yet, they were such a perfect example not only of junk DNA, but even of “errors” in DNA: a wonderful demonstration that evolution is unguided, non intelligent, egoist, and so on…

    What a pity!

  2. 2

    GP…what will someone, perhaps like Art Hunt, say about this?

    And isn’t Moran a staunch Junk DNA junkie?

  3. Upright BiPed:

    Yes Moran and Matheson and Hunt have recently committed themselves very much to that view (which I appreciate, I have often said, and it is no joke, that a good traditional neo-darwinist is by far better than an elusive revisionist neo-neo-darwinist).

    I don’t think that Moran and Matheson are looking forward to discussing that with us (but some volunteer could make a sacrifice and start monitoring PT). But maybe Artur Hunt, aho has demonstrated a really correct approach here, could be tempted to comment…

  4. Art hunt, Steve Matheson and Larry Moran all have blogs that accept comments. Go to it Gpuccio!

  5. This is ironic to say the least. :D

  6. Daniel Powter-Bad Day (lyrics)
    http://www.youtube.com/watch?v=RmNTAvnSais

  7. I particularly liked this quote from the abstract:

    However, given that microRNAs bind to RNAs, we hypothesized that RNAs could possess a regulatory role that relies on their
    ability to compete for microRNA binding, independently of their protein-coding function.

    I like it because: (1) it indicates that they were thinking in a strictly logical/engineering mode, rather than being dominated by Darwinist thought, and (2) it reminds me of some of things that have been posted here at UD over the last two years or so—Design logic.

  8. I’m confused.

    Isn’t the supposed “bias of Darwinism” supposedly preventing researchers from studying junk DNA?

    For example, if the claim that biologists commit the fallacy of assuming genes with no currently known function really are universally functionless was true, it’s unclear why anyone bothered to study these psuedogenes in the first place.

    As such, wouldn’t this be a “very bad day” for those who continually, perpetuate, these claims, despite research such as this which clearly suggests otherwise?

  9. great job and congrats to the ID movement for getting some science done that exposes the role of “Junk DNA”. Was this done through Dembski’s research program or is there another one? I’m a little out of the loop on where the research is being done.

    Thanks!

  10. A few questions.

    1. PaV said:

    >Yes, “junk” DNA now “communicates” with itself. A new “language”, an RNA language, is discovered. Another 30,000 pieces of functional information (over and above proteins) are part of cell architecture.

    Um, I count 12 (or thereabouts) objects of study in the cited paper. Even if we count every miRNA target site in these as a separate “piece of information”, I don’t see how we get to 30,000.

    2. Just how much of each pseudogene actually participates in the described decoying?

    3. If one does an informational inventory, I am pretty sure one will find that this mode of regulation is pretty unfriendly to ID, what with its insistence on high amounts of information and inaccessibility to random processes (neither of which applies to miRNA decoying by pseudogenes). So, the question is, why bring up the subject on this blog?

  11. veilsofmaya, Fross:

    Maybe the control of darwinism on research is not yet total. Somebody escapes, here and there. They must only be careful not to name ID in their papers.

    Maybe darwinists censors just use some google-like search engine to detect forbidden keywords (ID, design, intelligent), and if one is smart enough one can even publish papers which could “indirectly” favour ID. Maybe we are not in a totalitarian cognitive regimen, but only in a quasi-totalitarian one.

    Maybe there is still hope… If I were in the shoes of darwinists, I would definitely be worried :) .

    And, Frost: I have said that many times, and I say it again: it is not important “who” discovers the facts, but the facts themselves. Facts are nobody’s property. Science is a collective search for truth about reality. Both the search for facts and the discussion about known facts have their important roles.

    This is not a race to copyrights, I believe…

  12. veilsofmaya [8]:

    Isn’t the supposed “bias of Darwinism” supposedly preventing researchers from studying junk DNA?

    Did the Ptolemaic system of astronomy cause the ancients to stop studying the sky? Of course not. It just prevented them from attaining a proper understanding of what they were studying.

    Fross: Did biology, as a science, exist before 1859? IOW, are you saying that unless Darwinism is embraced then biology cannot truly function as a science?

    The driving force behind ID is simply the sophisticated lab methods now employed and the tremendous complexity they reveal. Have you ever heard of a paradigm shift?

  13. veilsofmaya @ 8:

    Those who continually perpetuate these claims include the New Scientist, where you can read this:

    Once the vast majority of our DNA was dismissed as junk, but now we know it is important – or so you might have read recently. In fact, it still appears likely that 85 to 95 per cent of our DNA is indeed useless. While many bits of DNA that do not code for proteins are turning out to have some function or other, this was predicted by some all along, and the overall proportion of our DNA with a proven function remains tiny.

    The article came out just last week. Here is a link for you to read more. Once you have a retraction of these false claims by the editors, give us a shout.

    http://www.newscientist.com/sp.....man-genome

  14. Crevo has a article up on the “Pseudogene” paper:

    The RNA Code: Pseudogenes Functional, Help Prevent Cancer
    Excerpt: The commentary began by calling it “surprising news” that “pseudogenes are functional and could have a role in the control of cancer.” While Rigoutsos noted that “pseudogenes have been presumed to be largely vestigial ,” he pointed to other recent findings that they are functionally connected to other RNA regulatory elements. In the same News and Views article, and Frank Furnari (UC San Diego) said this:

    Defining ‘junk DNA’ is getting trickier. Pseudogenes, for instance, have been viewed as non-essential genomic elements and have mostly been ignored. Well, they shouldn’t be anymore, according to Poliseno and colleagues, who show a clear functional relationship between the tumour-suppressor gene PTEN and its pseudogene PTENP1 (Fig. 1). This study could have major implications for understanding mechanisms of disease, and of cancer in particular.

    Furnari also pointed to other possible diseases where breakdown of the tight regulation of the PTEN could be responsible. Two of those are human breast and colon cancers. He said it may be time for a “redefinition of this seemingly vestigial pseudogene as a tumour-suppressor gene.”
    http://www.creationsafaris.com.....#20100624a

  15. @gpuccio (#10)

    Are you claiming this researchers are actually pro ID, but operating under the radar out of fear of being censured? If so, please indicate how you’ve reached this conclusion.

    I’m asking because the study of alternative functions of non-coding DNA is not exclusive to those who support ID. Nor is it necessary for junk DNA to be universally non-functional to collaborate evolution.

    Clarifications in this regards have been made time and time, again, which are ignored.

  16. @PaV (#11)

    PaV,

    And what factors prevented them from accepting Heliocentrism? Intuition, a conflict with the current day interpretation of scripture and personal incredulity.

    Please see here and here.

    @Alex73 (#12)

    Please see the clarification links in my previous comment. The term Junk DNA is used in the context which we commonly use the term junk.

    For example, I have a few of items that did one perform a function, some of which still may work. However, I no longer use them and I keep them around for sentimental value. If someone called them junk, I would not be offended because I understand the context by which they were using the term. I’ve kept them around, despite the fact that they currently do not serve a functional purpose.

    Nor does this refer to an assertion of universal non-function or some vague function as Matheson elaborates using the following analogy.

    Paint cans are sometimes found in piles of rubbish in vacant urban lots (VULs). Paint cans can be used to prop up old cars, or to fight off intruders, or to make music. Therefore VULs are useful in auto repair, home security, and musical composition.

    As such, Junk DNA is a way of referring to a specific class of genes that are currently thought to be non-coding. This is non-controversial, yet brought up by ID supporters time and time again.

    That anyone says some Junk DNA is non-functional is a like saying some of the genes of class Z are non functional. There is no necessary assumption that genes in class Z are universally non-functional. Attempt to conflate the class of junk DNA with universal non-function are disingenuous and opaque.

    Given the clarifications above, it would appear that ID proponents are merely offend by the very idea of the word “junk DNA” for reasons which would be obvious. God doesn’t make “junk” and the designer ID is referring to is God.

  17. @BornAgain77,

    It seems you’ve made my point for me.

    Given the clarifications above, none of these things in the post you linked to are controversial. The “problem” is one that ID’ists manufacture to suit their agenda.

  18. veilsofmaya :

    “I’m confused”

    Well that part is certainly clear enough.
    Most Darwinian fundamentalists are.

  19. As a religious studies major, I was excited by this post and emailed this to a biologist friend of mine as soon as I saw it here.

    He laughed at it and said that only a tiny bit of junk dna is pseudogenes, only a minority of pseudogenes are expressed as rna, and this paper was only about one pseudogene.

    He also made the same observation that the darwinists did here, that it disproved any claims about bias.

    So I felt embarrassed and had no good response. How should I have responded to his points?

  20. veilsofmaya (#14):

    I would like to clarify my personal positions about this subject:

    1) Pro ID or non pro ID research:

    You say:

    Are you claiming this researchers are actually pro ID, but operating under the radar out of fear of being censured? If so, please indicate how you’ve reached this conclusion.

    I don’t know and I don’t care. Other researchers have IMO been pro ID, and have operated for some time with what we could call “reasonable caution”. Of these reasearchers I know nothing, and they probably have nothing to do with ID.

    But that is not the point. The point is that, as I have always openly stated, research in itself is neither pro ID nor against ID, as long as it finds true facts and data. Let’s say it is pro scientific knowledge.

    Obviously, the inspiration of research and the interpretation of the results are usually done according to one’s paradigm: as ID and darwinism are antagonistic paradigms, the interpretation of scientific results, or at least of some of them, is different in the two fields.

    But, as I firmly believe that ID is the best theory, I always welcome all new findings, confident that, beyond the first partial interpretation of them made by official darwinist biology, in time they always reveal their importance for ID.

    What I have never understood is the arrogant position of some darwinists who think that the results of research in some way “belong” to darwinism because the scientists who obtained them adopt a conventional “darwinist” approach. That is not true. Facts belong to all.

    So, when you say:

    I’m asking because the study of alternative functions of non-coding DNA is not exclusive to those who support ID.

    I obviously agree with you.

    2) The relationship between the concept of junk DNA, darwinism and ID.

    That’s more tricky. You say:

    Nor is it necessary for junk DNA to be universally non-functional to collaborate evolution.

    To a point, I can agree with you. The problem of non coding DNA is not essential neither to ID nor to darwinism. But some facts are certainly true:

    a) Coventional darwinism has freely chosen to interpret non coding DNA as “non functional”. More than that, it has been considered as “evidence” of non intelligent evolution.

    b) Many important darwinist biologists ((Moran, Matheson, Hunt), even today, believe that most non coding DNA is non functional, and argue in that sense. Again, their choice.

    c) I have never believed that non coding DNA is non fucntional. While this instinctive conviction can be partially related to my ID approach, it more explicitly derives from two facts:

    - I have never considered credible that 95% or more of the human genome is non functional. That concept seems so ridiculous that I have never seriously considered it as true. Call it an argument for incredulity A good argument form incredulity.

    - I have always been aware of the important problem, many times discussed here, which I call “the problem of the missing procedures”. IOW, I always thought that the protein coding genes were only the gross effectors of biological information, but that all the fine regulatory software, the “procedures”, were missing. So, I always thought that non coding DNA (95% of the human genome of which we don’t understand the function) was a very good candidate for at least part of that information. I believe that all the evidences that have accumulated in recent yeras, and continue to accumulate about this subject, are a very good confirmation of that idea.

    d) So, finally, is the function of non coding DNA a falsification of darwinism?
    No, it isn’t. But it is certainly a falsification of some very silly interpretations made by some darwinists, and encouraged by the possible support that those interpretations could give to the main theory. Moreover, the new functions discovered for non coding DNA certainly “make things more difficult” for darwinian theory. Indeed, any new level of functional complexity which is daily discovered in living beings has that effect, because the greatest weakness of darwinism is that it is utterly incapable to explain functional complexity.

    So, the more the functional complexity, the more the difficulties for darwinism. Especially if that complexity is multilevel, stratified, regulatory, integrated, realizing increasingly growing networks of software-like information whose existence was not even suspected 10 or 20 years ago.

    Therefore, I do believe, today like years ago, that most of non coding DNA will be found to be functional, and highly functional. And that includes probably all types of it: introns, transposons, pseudogenes, and so on. Is such a non protein coding function a falsification of darwinism? Not especially. Not alone.

    But it does help!

  21. Joaozinho:

    He laughed at it and said that only a tiny bit of junk dna is pseudogenes,

    That’s true, but there are growing evidences for regulatory fucntions of the other parts too (like introns). Pseudogenes are only the new entry.

    only a minority of pseudogenes are expressed as rna,

    That’s absolutely not known.

    and this paper was only about one pseudogene.

    True, but this paper is only the beginning. The approach is new, just wait and see.

    He also made the same observation that the darwinists did here, that it disproved any claims about bias.

    What does that mean? Please, explain. We IDists are notoriously not intelligent…

  22. Intelligent design cannot explain the presence of a nonfunctional pseudogene, unless it is willing to allow that the designer made serious errors, wasting millions of bases of DNA on a blueprint full of junk and scribbles. Evolution, however, can explain them easily. Pseudogenes are nothing more than chance experiments in gene duplication that have failed, and they persist in the genome as evolutionary remnants…

    Ken Miller

    ROTFL

  23. 23

    Interesting the ways in which materialist try to rewrite/deny the written history of thought as it concerns junk DNA.

  24. gpuccio, thanks for your reply.

    When you say growing evidences, what do you mean exactly? That most of junk dna is now accounted for?

    And if the amount of pseudogenes that are expressed is absolutely not known, isn’t it deceptive to use this as an example? I’m asking this because I feel like I am being left without an IDist leg to stand on.

    My friend, who is a genome scientist, asked me to ask you how much you are willing to bet that there have been no surveys of pseudogenes to see if they are expressed—I think he used the word transcribed.

    What I meant about his observation was that it disproves the claim that ID-friendly research cant be funded or published.

  25. Joaozinho does this help?

    How The Junk DNA Hypothesis Has Changed Since 1980 – Richard Sternberg – Oct. 2009 – Excellent Summary
    Excerpt: A surprising finding of ENCODE and other transcriptome projects is that almost every nucleotide of human (and mouse) chromosomes is transcribed in a regulated way. http://www.evolutionnews.org/2.....is_ha.html

    here is another gem from Crevo:

    Pier Paolo Pandolfi of BIDMC explained, “This means that not only have we discovered a new language for mRNA, but we have also translated the previously unknown language of up to 17,000 pseudogenes and at least 10,000 long non-coding (lnc) RNAs.
    http://www.creationsafaris.com.....#20100624a

  26. 26

    “Are you claiming this researchers are actually pro ID, but operating under the radar out of fear of being censured? If so, please indicate how you’ve reached this conclusion.”

    I wont speak for GP, but I have personally interacted with researchers that did exactly as you say. I once emailed an author of a published paper and asked him to clarify a topic in his research. I told him I did not know his metaphysics and did not care to know, but admitted that I was pro ID and then asked the question I wanted clarified. He emailed me back the answer, which then lead to follow up email by me.

    He then sent me an email and said that he would follow up, but preferred to use regular mail. Several days later I received his letter. In that letter he was clear about his thoughts, and asked for confidentiality (which was already a given). And then – get this – he asked me to destroy the envelope he had used to mail the response.

    - – - – - – -

    Materialists like to pose such questions as the one above. They like to spit challenges at anyone who would dare to observe them as they very often are. They dismiss their intolerant hegemony in one breath then talk of consensus in the next.

    It won’t last though. That’s what facts are for.

  27. bornagain,

    Yes, it helped me to see that my friend was right about everything.

    First, gpuccio was gracious enough to politely point out PaV’s exaggerations.

    Then, you did exactly what my friend predicted someone would do—try to pass off transcription as sufficient to demonstrate function.

    I’m really disappointed.

  28. But Joaozinho you stated:
    “My friend, who is a genome scientist, asked me to ask you how much you are willing to bet that there have been no surveys of pseudogenes to see if they are expressed—I think he used the word transcribed.

    and I gave you this:

    A surprising finding of ENCODE and other transcriptome projects is that almost every nucleotide of human (and mouse) chromosomes is transcribed in a regulated way.

    Thus I gave you exactly what you had asked for Joaozinho, and by the way Joaozinho transcription is in fact completely unexpected from the neo-Darwinian framework. And is indeed a very strong indication of function though we are just barely beginning to understand the unmatched complexity being revealed in the genome,, that was what was completely surprising about the ENCODE study! That you would imply I was misleading you by implying function is disingenuous to what you actually asked for and what I actually gave you and is also misleading to what the current state of the evidence is for Intelligent Design framework to the neo-Darwinian framework. frankly if I had wanted to impress you with 100% functionality, that teams of leading scientists can’t even fully unravel, I would of used recent proteome studies.

  29. bornagain,
    When you are in a hole, quit digging.

    You did not give me what I asked for. The function discovered in this case required transcription, but transcription is not sufficient to assume function. Even I can see that this would not have been a Nature paper if they had just shown transcription.

    Clearly, if a pseudogene is not transcribed/expressed, it can’t possibly have the function that PaV was generalizing from.

    I’m not being disingenuous here. I came here looking for answers, not further exaggerations.

  30. Joaozinho:

    Please, greet your friend for me :) -

    All the best.

  31. Joaozinho:

    Let me ask you a simple question. Do you think 20,000-30,000 genes is a sufficient amount of information for a complex organism such as a mammal?

  32. Art Hunt[10]:

    Read the PhysOrg link:

    This means that not only have we discovered a new language for mRNA, but we have also translated the previously unknown language of up to 17,000 pseudogenes and at least 10,000 long non-coding (lnc) RNAs. Consequently, we now know the function of an estimated 30,000 new entities, offering a novel dimension by which cellular and tumor biology can be regulated, and effectively doubling the size of the functional genome.”

    The fact that the authors are speaking of a new genetic “language” is very problematic for Darwinism: Darwinism can’t answer the question, Whence the DNA code? Now it has to answer another question: Whence the RNA code?

    And, if that weren’t bad enough, the supposed uselessness of pseudogenes is now demonstrated to be in error. See Sal’s quote from Ken Miller.

    As I posted, “Another Bad Day for Darwinism”!

    veilsofmaya [16]:

    And what factors prevented them from accepting Heliocentrism? Intuition, a conflict with the current day interpretation of scripture and personal incredulity.

    Your initial argument ran roughly like this:

    “PaV says that the bias of Darwinism blinds researchers to the function of junk DNA. Yet the researchers are studying junk DNA. If they thought it had no function, then why are they studying it.”

    In invoking Ptolemeyism, I was pointing out that though the astronomers were wrong in their understanding of planet motion, this didn’t stop them from studying the motion of planets.

    You didn’t respond to this point I made. Instead, you sped forward to the Copernican revolution (BTW, you do know, of course, that Copernicus was a Catholic cleric? See here) and now want to infer that it is perfectly permissible to draw an analogy between that paradigm shift and the current one taking place, implying that ID thinkers are blinded in some way. But you invoke a two-edged sword. And the “scripture” of today is Nature magazine. And the chief high priests are the evolutionary biologists. And they make sweeping statements like “nothing in biology makes sense without the theory of evolution” (meaning Darwinisms). So, your attempt at smearing gets you nowhere.

  33. Arthur Hunt (#10):

    Um, I count 12 (or thereabouts) objects of study in the cited paper. Even if we count every miRNA target site in these as a separate “piece of information”, I don’t see how we get to 30,000.

    Again, the point is: functional modalities are being discovered for what was considered non functional DNA. That will go on. There is no reason to just count what is known and stick to the point that there is still much unknown to affirm that it will remain unknown, or that there is nothing to know. Our point is: we are beginning to understand, that’s only the beginning.

    Just how much of each pseudogene actually participates in the described decoying?

    Again “how much”. I don’t think that’s a good way to be quantitative. We are discovering informational networks. Only a little bit of them. Some parts work in a way, other parts will be probably shown to work in another way. That’s complexity.

    If one does an informational inventory, I am pretty sure one will find that this mode of regulation is pretty unfriendly to ID, what with its insistence on high amounts of information and inaccessibility to random processes (neither of which applies to miRNA decoying by pseudogenes). So, the question is, why bring up the subject on this blog?

    I disagree. While the comnplexity of regulatory networks is certainly more difficult to assess than the complexity of a single protein domain, it should be obvious, and it will be demonstrates in tfime, that regulatory networks are even more unlikely to arise by chance and necessity than “simple” first level structural information. On what do you base your statement that “this mode of regulation is pretty unfriendly to ID”? Not again, I hope, on your point that biological machines are different form mechanical machines? I have already answered that elsewhere, but if you want we can take again the discussion here.

  34. PaV,

    As I look through the abstracts for the RNA 2010 meeting in Seattle, I find lots of stuff that reveals the quotes you bring up to be incredible hyperbole. The authors’ findings do not apply to many long ncRNAs (look up some work on these – you’ll find lots of stuff that has nothing to do with miRNA decoying), and they don’t apply to the thousands of pseudogenes that are not transcribed to any great extent. (Please spare us the “95% of the genome is transcribed” line – the transcripts IDists are so excited about are so exceedingly rare that they cannot possibly be involved in miRNA decoying.) In a nutshell, their extrapolation is unwarranted and has already been refuted by numerous studies.

    Then there is the fact I see has been ignored – that this mechanism for regulation is quite unfriendly to ID.

  35. veilsofmaya:

    Given the clarifications above, it would appear that ID proponents are merely offend by the very idea of the word “junk DNA” for reasons which would be obvious. God doesn’t make “junk” and the designer ID is referring to is God.

    You have a point here, but not the way you think. Junk DNA is compatible with Darwinism, because it fits the result of an unguided and unintelligent process. Perfect DNA is also compatible with Darwinism, after all, nature had 4+ billion years to make it perfect. (Actually, both of them are also compatible with ID, in its purest form, because not everything has to be designed.)

    Why is it then, that Darwinists trumpet that DNA is junk? Why is it that they blatantly allow unjustified leaps of logic to declare something useless, when the we just simply do not understand it? They are intelligent scientists and not so dull that they would not see the trivial flaws in their arguments.

    It is because, junk DNA, or at least wast amounts of junk DNA is not compatible with an omnipotent, omniscient and good Creator, described in the Bible. The main purpose of Darwinism is to prove the Bible and its historic account false. Once that is done, the moral code described there is also meaningless, so we can do whatever we feel all right. In this battle anything is permitted, because the vast majority of the public will not understand or dare to question those in white lab cloaks.

    Is the inverted retina unexpected at first sight? Shout it out loud: God would have made it better! Leringeal nerve goes in an unusual path? Stuuuuupiiiid designnnn! Large parts of DNA do not code proteins? Junk, junk, junk!!!!!

    Truth does not matter here. (It eventually comes to the surface when our puny knowledge is somewhat increased and become able to appreciate these solutions.)

    Darwinist journalism is not science, but evangelism for atheism.

  36. Joaozinho you suggest to me:

    “When you are in a hole, quit digging.”

    Which is also known as the first law of holes:

    It is a good thing to follow the first law of holes; if you are in one, stop digging.
    [1988 D. Healey Observer in J. Care (ed.) Sayings of the Eighties]

    But Joaozinho am I really in a hole? foras to PaV’s cite from the Physorg article in post 32,,,,

    This means that not only have we discovered a new language for mRNA, but we have also translated the previously unknown language of up to 17,000 pseudogenes and at least 10,000 long non-coding (lnc) RNAs. Consequently, we now know the function of an estimated 30,000 new entities, offering a novel dimension by which cellular and tumor biology can be regulated, and effectively doubling the size of the functional genome.”

    ,,,,, thus it appears that neo-Darwinists are the ones that are actually in the hole futilely digging themselves deeper. I am quite comfortable with the Intelligent Design postulation of “Junk DNA” being functional and see absolutely nothing in the article that would go against that postulation. I am just left wondering why your friend would “laugh” at such a profound breakthrough as discovering another “language” within the DNA. Does he have some sort of compulsion to dig holes?

    Dig it – From the Disney Movie “Holes”
    http://www.youtube.com/watch?v=ybjSSExktzI

  37. 37

    I don’t get this. I’ve read the OP and tried to read the article it references even though it appears to be written in another language.

    As far as I can tell from the discussions at the end of the article, a former gene which has been mutated into disfunctionality (a pseudogene) has picked up a second function, unrelated to the first.

    But isn’t this exactly what evolution says happens? A gene is duplicated, a mutation disables one copy and then the remainder is available for a new function. How is this “bad for Darwinism”? It looks more like a confirmation of evolution to me.

  38. Let’s call it the Great Divergence. These poor authors weren’t trying to disprove evolution. They are probably evolutionists themselves. They were simply looking at nature for its own sake, without Darwin’s rose-colored glasses.

    Something interesting is happening in the hard sciences. The tests have become so sophisticated that they have slipped the surly bonds of Darwinism. Basic research, not driven by any agenda, is taking the human race on a fantastic voyage of discovery. The more we know, the more we realize that nature is highly complex and functional in astonishing ways.

    This is “bad news” for Darwinism because Natural Selection requires nature to be rather simple. One can, on a dreamy summer evening, imagine the poor girl creating herself through deep time if she doesn’t have very much to do. But each new study finding makes Darwin’s theory look increasingly anthropomorphic. Natural Selection attributes a degree of creativity and ingenuity to nature that cannot be found in nature itself; that exceeds nature’s natural limitations.

    The worker bees of science have been casting light (unintentionally) on a disconnect between the grand, unifying theory and the particulars of experience. The vestiges of language and purpose they uncover indicate something very different from what Darwin had in mind. Do their discoveries disprove his theory? No; that’s the genius of Darwin. Virtually nothing can disprove his theory. Will Darwinism go away? Not as long as there are people who want to believe it.

    But basic science is making it possible to become an intellectually fulfilled believer again. What we see with our own eyes and what the Darwinists want us to believe about the nature of being are two very different things. Nothingness is overthrown, and with it the arrogance of those who sought to put themselves in the place of God.

  39. gpuccio: Please, greet your friend for me -

    All the best.

    I will. He was sure that you wouldn’t accept his bet.

    Phaedros: Let me ask you a simple question. Do you think 20,000-30,000 genes is a sufficient amount of information for a complex organism such as a mammal?

    Of course not! They are meaningless outside the context of the cell and embryo. That is where I find space for ID, not in the genome.

    gpuccio: Again, the point is: functional modalities are being discovered for what was considered non functional DNA. That will go on. There is no reason to just count what is known and stick to the point that there is still much unknown to affirm that it will remain unknown, or that there is nothing to know. Our point is: we are beginning to understand, that’s only the beginning.

    But isn’t that why the evolutionists are studying this, that they are sure enough that some of what is provisionally classified junk will have function?

    My question is, how much of the genome is accounted for? That’s where I feel deceived by the OP, and it’s where I appreciate your honesty, gpuccio.

    bornagain: But Joaozinho am I really in a hole?

    Yes, you really are. Are you willing to take my friend’s bet?

  40. chrisvander:

    As far as I can tell from the discussions at the end of the article, a former gene which has been mutated into disfunctionality (a pseudogene) has picked up a second function, unrelated to the first

    That’s how a darwinist would try to explain what is observed. What is observed is that a copy of a very important gene, having been translation inactivated, is anyway transcribed, and the transcribed mRNA acts as a fine regulator of the original active gene. From an ID point of view, that’s a very intelligently integrated and finely tuned system.

    Moreover, the pseudogene in reality has not picked up a second function, as assumed by the imaginative darwinist principle of cooption. Instead, it’s exactly because the pseudogene is highly homologous to the original gene that it can work to regulate it, through the means of the miRNA network.

    So, a specific functional sequence is used both to produce its protein and, after appropriate inhibition of translation, to regulate that production.

    But isn’t this exactly what evolution says happens?

    No, it’s exactly what we would expect from a very sophisticated design. The conservation of the basic sequence allows the miRNA competition, while the inactivation of the translation ensures the regulatory fucntion. A finely tuned balance between homology and difference is here the key to reach a finely tuned result.

  41. Art, we weren’t talking about your upcoming conference.

    And we’re all entitled to our own opinions. You seem to have a conception of how information works, or doesn’t work, that differs radically from most of us here. You’re free to do so. But that doesn’t make it science. It’s just opinion.

  42. Joaozinho you asked:

    My question is, how much of the genome is accounted for?

    Depending on your level of “proof” for functionality, which seems to be quite high since you want to know “complete” functionality, it varies substantially thus since I maintain that most all of the “Junk DNA will be found to have function, I want you to pick a number, any number for what you think the percentage of Junk DNA is,,,

    Asking Darrel Falk to Pick a Number, Any Number
    http://www.evolutionnews.org/2.....32871.html

    Sternberg excerpt:

    Now, the problem with such a statement is this: While there are ~25,000 protein-coding genes in our DNA, the number of RNA-coding genes is predicted to be much higher, >450,000.1 Some of the latter range in length from being quite short—only 20 or so genetic letters—to being millions of letters long. Since 2004 we have learned that over 90% of our DNA is transcribed into RNA sequences at some developmental stage, in different cell and tissue types.2, 3, 4 (Our brain cells are unusually rich in these non-translated RNAs.) These RNAs are then processed into regulatory and structural sequences of all sizes.2, 3, 4

    It could of course be argued, as it has been, that most of these RNA transcripts are themselves junk. But a host of them are packaged into complexes with different proteins.1

    So the true number of genes in our DNA is probably >450,000 + 25,000 = >475,000. What is more, these >450,000 genes cover more than 88.5% of our 3 billion genetic letters. That’s right—most, if not close to all, of our chromosomal DNA consists of different types of genes that have only recently been discovered.

    How do these facts square with this comment made by Falk?

    “but this still doesn’t negate the fact that almost certainly much, if not most, of the DNA plays no role, and in many cases can be harmful.”

    Well, it all depends on how he is using the words “much” and “most.” I really don’t know. So I have a question for him: Exactly what fraction of the transcribed 88.5% of our DNA are you willing to say “plays no role” or can be harmful? All I am asking for is a prediction, such as “90% of these DNA letters is superfluous” (“or 79.5% of the RNAs are nonsensical”). Since he also said “almost certainly” in the above statement, he must have a figure in mind. So I say pick a number, any number…But to be a good sport, I’ll show my prediction: All of the expressed 88.5% of our DNA has diverse roles in our development.

  43. Arthur Hunt (#34):

    Then there is the fact I see has been ignored – that this mechanism for regulation is quite unfriendly to ID.
    I have not ignored

    As you can see in my #33, I have not ignored that statement of yours. And again I ask you: why? Let’s discuss this interesting point (it’s a serious invitation).

  44. 1. Some numbers, for a proper perspective:

    Conservative estimate number of bp in the human genome that is not protein-coding or stable RNA (a very generous estimate for anti-junkites) – 2,400,000,000

    Number of nts involved in miRNA decoying (per decoy site) – ca. 25

    Maximum number of bp “covered” by the (wildly optimistic) claims of the PhysOrg article – 750,000

    Percentage of “junk DNA” that the article cited by PaV eliminates – 0.03.

    I’d say that we haven’t made any dent at all in the “junk DNA” problem. And that’s before we correct the hyperbole in the cited article.

    2. About my claims about information and functional pseudogenes:

    Recall that a pseudogene is the product of a duplication event. In my experience, ID proponents are rather insistent that duplications do not add new information to the genome. So a functional pseudogene is the product of an information-neutral event.

    Except that it really isn’t. Because the pseudogene must undergo some mutational changes that eliminate the possibility of translation. In my experience, ID proponents are rather insistent that such mutations are actually losses of information. So the bottom line is that functional pseudogenes are the results of losses of information. (Don’t ask me to make sense of this – I’m just following the trail of ID logic here.)

    We know how genetic duplications occur – they are the results of typical biochemical processes, and they are, for all intents and purposes, random and unguided. Which means that functional pseudogenes are, for all intents and purposes, the results of random processes that reduce information content.

    In other words, new layers of regulation arise from random events that most definitely do not increase information contents of genomes. As I was saying, this is not exactly something that is friendly to ID.

  45. Arthur Hunt:

    Thank you for elucidating your thought. My comments:

    1) On the quantitative issue. The important point, IMO, is not “how many nucleotides” are involved in the miRNA competion (I happily accept your calculation), but that a specific subset of “junk” DNA, pseudogenes, which have been traditionally considered mayube the most evidently “error-like” part of non coding DNA, are now shown to be functional, and part of a very complex and integrated regulatory network. We know very well that pseudogenes are only a minority part of non coding DNA, but conceptually they are a very important subset. Other parts of non coding DNA have alredy been shown to be functional in different ways (see our previous discussion about introns), and I am sure that new modalities of function (probably many of them) will be elucidated in a very short time (as research seems now top be justly alerted to these new frontier of knowledge). So, again, I have nothing against your “quantitative” approach: if you want each time a new modality is discovered to count the single nucleotides involved, and stick to how many are still not explained as functional, that’s fine form me, but essentially I don’t believe that’s the right way of getting the real picture.

    2) This is more interesting. I believe you really misunderstand the ID point. Let’s see:

    Recall that a pseudogene is the product of a duplication event. In my experience, ID proponents are rather insistent that duplications do not add new information to the genome. So a functional pseudogene is the product of an information-neutral event.

    That’s not completely correct. It is true that a duplication event in itself adds no new information with respect to the sequence itself which is duplicated. For instance, if we are analyzing a causal scenarion where a transition is supposed to happen form one duplicated protein A’ to a new protein B, through RV and NS, the act of duplication in itself is not a step towards the new sequence, except for the fact that it can provide a non functional copy of A which can vary without being affected by negative selection (if A’ is not translated). So, even in this case there is a variation in the information content of the whole system, if not in the sequence.

    Let’s go to our model of duplication as a pathway to regulation (which is obviously different from the model of duplication as a pathway to a new functional primary sequence).
    Here, there is a lot of information change implied in the duplication event, and in the following events:

    a) which gene is duplicated (of all possible gene duplications)

    b) where it is duplicated

    c) which parts of UTRs or other flanking regions are duplicated

    d) which parts of the duplicated gene are not homologous to the original gene, both in the coding and non coding sequence

    e) how many duplicated genes exist of that particular gene, and how different they are one from the other

    f) whether the duplicated gene is translated

    g) whether the duplicated gene is transcribed

    h) how much the duplicated gene is transcribed, and how its transcription is regulated in relation to the original gene’s transcription

    i) how many miRNA sites are retained, and which, both in the coding and non coding region, and the individual role of each of those miRNA in regulation

    j) how much the interaction between the pseudogene mRNA and miRNAs influences other genes, and which.

    k) other possible effects of the pseudogene mRNA, at present not known

    And so on.

    My point is, if we believe that transcription and translation of the original gene are finely regulated by a complex network, including miRNAs (and many other regulatory modalities), then the duplication-mutation event must be finely tonuse to integrate in such a network. The point is not that the event in itself is “possible” through known random biochemical mechanisms. It certainly is, exactly as the mutations which can bring to a new functional protein are certainly “possible” from a biochemical point of view.

    The ID point is that such events are rare functional examples among a huge majority of non functional possible events. The ID point is that, exactly as obtaining a new functional protein is empirically impossible through RV and NS alone, in the same way obtaining a finely tuned duplication, or set of duplications, and the coordinated mutations both in the coding and non coding sequence and in the related regulatory sequences, which perfectly integrates in a complex regulatory system involving many different agents, is empirically impossible through RV and NS alone.

    Here, while the sequence information varies relatively little (but not really little), differently form what happens when a new protein domain appears, the information in the whole regulatory network changes very much. The problem is that analyzing the information content of a complex regulatory network is much more difficult then analyzing the information content of a primary sequence, especially when the regulatory network is only very partially understood. That’s the only reason why ID has focused the attention more on basic protein structures, and less (for the moment) on regulatory networks.

    But, as our understanding of regulatory networks increases, a quantitative analysis of their information content will follow.

    Except that it really isn’t. Because the pseudogene must undergo some mutational changes that eliminate the possibility of translation. In my experience, ID proponents are rather insistent that such mutations are actually losses of information. So the bottom line is that functional pseudogenes are the results of losses of information. (Don’t ask me to make sense of this – I’m just following the trail of ID logic here.)

    From what I have said before, it should be clear that the mutation which disactivates translation is part of a set of coordinated changes which add a specific regulatory function to the system. There is a lot of sense in that.

    We know how genetic duplications occur – they are the results of typical biochemical processes, and they are, for all intents and purposes, random and unguided. Which means that functional pseudogenes are, for all intents and purposes, the results of random processes that reduce information content.

    I disagree. We have no evidence that those “typical biochemical processes” are random and unguided, any more than we have evidence that all single point mutations are random and unguided. One of the most likely scenarios for ID is the existence of guided RV. Moreover, many pseudogenes are the result of transposon activity, and transposon activity is a very good candidate as an interface for guided variation.

    IOW, the main point of ID is that the results usually ascribed to RV and NS are best explained by designed guided variation and/or designed intelligent selection.

    In other words, new layers of regulation arise from random events that most definitely do not increase information contents of genomes. As I was saying, this is not exactly something that is friendly to ID.

    And,from what I have said, that is not true: the ID point is that those new layers of regulation arised from design, and that it is empirically not credible that they could arise differently: the facts of pseudogene function are very well explained by an ID scenario, and totally “ID friendly”.

  46. gpuccio, I think you may find this paper that just came out interesting:

    Messenger RNAs are regulated in far more ways than previously appreciated, study finds
    Excerpt: A team of molecular biologists from Cold Spring Harbor Laboratory (CSHL) has now discovered that mRNAs can be targeted for destruction by several modes and molecules, highlighting a previously unanticipated complexity in the control and regulation of the cell’s genetic messages.
    http://www.physorg.com/news196687864.html

  47. Arthur Hunt,

    On top of the penetrating questions gpuccio brings to you for the inadequacy of neo-Darwinism to account for the origination of “higher level” regulatory functions in the genome, my question is much more foundational to your position:

    How in blue blazes do you, as a neo-Darwinist, justify your belief that mutations to DNA is the main catalyst of the morphogenesis of new species, when genetic reductionism is falsified in the first place? And since genetic reductionism is falsified as being the “cause” of morphogenesis, how do you justify using purported genetic similarities as evidence for common ancestry?

    notes:

    Stephen Meyer – Complexity Of The Cell – Layered Information – video
    http://www.metacafe.com/watch/4798685

    …Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection.” – Jonathan Wells
    http://www.evolutionnews.org/2.....footnote19

    Darwin’s Theory – Fruit Flies and Morphology – video
    http://www.youtube.com/watch?v=hZJTIwRY0bs

    Hopeful monsters,’ transposons, and the Metazoan radiation:
    Excerpt: Viable mutations with major morphological or physiological effects are exceedingly rare and usually infertile; the chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event. These problems of viable “hopeful monsters” render these explanations untenable.
    Paleobiologists Douglas Erwin and James Valentine

    “Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find the information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing that there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype (Body Plan).” Michael John Denton page 172 of Uncommon Dissent

    “There is now considerable evidence that genes alone do not control development. For example when an egg’s genes (DNA) are removed and replaced with genes (DNA) from another type of animal, development follows the pattern of the original egg until the embryo dies from lack of the right proteins. (The rare exceptions to this rule involve animals that could normally mate to produce hybrids.) The Jurassic Park approach of putting dinosaur DNA into ostrich eggs to produce a Tyrannosaurus rex makes exciting fiction but ignores scientific fact.”
    The Design of Life – William Dembski, Jonathan Wells Pg. 50

    Stephen Meyer – Functional Proteins And Information For Body Plans – video
    http://www.metacafe.com/watch/4050681

    A comparative approach for the investigation of biological information processing: An examination of the structure and function of computer hard drives and DNA – David J D’Onofrio1, Gary An – Jan. 2010
    Excerpt: It is also important to note that attempting to reprogram a cell’s operations by manipulating its components (mutations) is akin to attempting to reprogram a computer by manipulating the bits on the hard drive without fully understanding the context of the operating system. (T)he idea of redirecting cellular behavior by manipulating molecular switches may be fundamentally flawed; that concept is predicated on a simplistic view of cellular computing and control. Rather, (it) may be more fruitful to attempt to manipulate cells by changing their external inputs: in general, the majority of daily functions of a computer are achieved not through reprogramming, but rather the varied inputs the computer receives through its user interface and connections to other machines.
    http://www.tbiomed.com/content/7/1/3

    Arriving At Intelligence Through The Corridors Of Reason (Part II) – April 2010
    Excerpt: In fact the term ‘junk DNA’ is now seen by many an expert as somewhat of a misnomer since much of what was originally categorized as such has turned out to be pivotal for DNA stability and the regulation of gene expression. In his book Nature’s Probability And Probability’s Nature author Donald Johnson has done us all a service by bringing these points to the fore. He further notes that since junk DNA would put an unnecessary energetic burden on cells during the process of replication, it stands to reason that it would more likely be eliminated through selective pressures. That is, if the Darwinian account of life is to be believed. “It would make sense” Johnson writes “that those useless nucleotides would be removed from the genome long before they had a chance to form something with a selective advantage….there would be no advantage in directing energy to useless structures”.

    further note:

    Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness – May 2010
    Excerpt: Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken.
    http://bio-complexity.org/ojs/.....O-C.2010.2

    This following paper reveals that there is a “cost” to duplicate genes that further precludes the scenario from being plausible:

    Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model
    Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence. http://www.springerlink.com/co.....4014664w8/

    Fearfully and Wonderfully Made – Glimpses At Human Development In The Womb – video
    http://www.metacafe.com/watch/4249713

    As you can see Arthur Hunt there are many intractable problems with your genetic reductionism scenario coming from multiple angles.

  48. A little more clarity:

    This inability of body plans to be reduced directly to the DNA code is clearly shown by Cortical Inheritance.

    Cortical Inheritance: The Crushing Critique Against Genetic Reductionism – Arthur Jones – video
    http://www.metacafe.com/watch/4187488

    “Live memory” of the cell, the other hereditary memory of living systems – 2005
    Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory.
    http://www.sciencedirect.com/s.....3daa6bdef8

  49. @Alex73 (#35)

    You wrote:

    Why is it then, that Darwinists trumpet that DNA is junk?

    Alex,

    You’re back to making ambiguous statements again. Darwinsts clearly do not claim that “DNA is junk”. Again, they use the term “junk DNA” to describe a specific class of bases that we currently think are not directly involved in coding.

    Why is it that they blatantly allow unjustified leaps of logic to declare something useless, when the we just simply do not understand it?

    Again, they do not suggest it is “useless” in it is universally non-functional. Nor do they suggest we may not find other functions for non-coding DNA. You seem to be conflating the class of junk DNA with universal non-function.

    Are you sure this isn’t just a reaction to being offended by even the hint of any sort of non-functionality in DNA?

  50. @gpuccio (#20)

    Thanks for your response.

    I have a few follow-up questions. You wrote..

    - I have never considered credible that 95% or more of the human genome is non functional. That concept seems so ridiculous that I have never seriously considered it as true. Call it an argument for incredulity A good argument form incredulity.

    First, when you say non-functional are you referring to universal non-function or having some indirect role in expression? If the former, then the 95%+ figure your using here is not applicable. Again, this really is non-controversial.

    However, I’m guessing you’d also find the idea that a even the rough estimation such as any significant part of the human genome was is universally non-functional is ridiculous as well. Correct? If so, it’s here that we would being to diverge.

    Given that the lungfish as 130 billon bases compared to the roughly 3 billon bases in human beings, what is the purpose of, lets say 70 billon of the 127 lungfish bases which humans being lack? That is, if your argument is from incredulity, what other “credible” explanation does Intelligent Design provide for why lungfish have 40 times the number of bases than we do?

  51. @gpuccio (#45)

    You wrote:

    The ID point is that such events are rare functional examples among a huge majority of non functional possible events. The ID point is that, exactly as obtaining a new functional protein is empirically impossible through RV and NS alone, in the same way obtaining a finely tuned duplication, or set of duplications, and the coordinated mutations both in the coding and non coding sequence and in the related regulatory sequences, which perfectly integrates in a complex regulatory system involving many different agents, is empirically impossible through RV and NS alone.

    Gpuccio,

    How is this not a convoluted elaboration of TOE?

    The complexity of biological life is just like neo-darwinsts suggest in that the arrival of harmful traits are unplanned errors on the part of nature, while the appearance of useful traits, including those that only appeared to be neutral or unhelpful on their own but add up to an advantage when put together, are really the work of an intelligent being. In other words, it’s like evolution, except an intelligent designer must have occasionally stepped in because useful traits represent information and information is defined as resulting from an intelligent agent, or you simply can’t imagine a way these traits formed naturally (personal incredulity.)

    Again, your’e drawing what appears to be an arbitrary boundary. We can understand how harmful traits appear, but no amount of problem solving or reasoning can explain how positive traits can appear.

  52. 52

    @Pav (#12)

    You wrote:

    “PaV says that the bias of Darwinism blinds researchers to the function of junk DNA. Yet the researchers are studying junk DNA. If they thought it had no function, then why are they studying it.”

    First, As I read it, your suggesting was it was “a bad day for Darwinism” because of the specific details of the discovery. That is, because you thought Darwinism could not explain it. While you may have made such an argument elsewhere or you thought it was implied, it was not explicitly present in your post. This is why I wrote..

    if the claim that biologists commit the fallacy of assuming genes with no currently known function really are universally functionless was true, it’s unclear why anyone bothered to study these psuedogenes in the first place.

    … and linked to specific arguments …

    As such, wouldn’t this be a “very bad day” for those who continually, perpetuate, these claims, despite research such as this which clearly suggests otherwise?

    … rather than making a blanket statement of ID as a whole.

    As such, your most effective response would have been to point out that the “bias of Darwinism” supposedly preventing researchers from studying junk DNA was a misrepresentation of your position. However, this particular argument was not explicitly present this particular position in this post.

  53. 53

    @Pav (#12)

    You wrote:

    You didn’t respond to this point I made. Instead, you sped forward to the Copernican revolution (BTW, you do know, of course, that Copernicus was a Catholic cleric? See here) and now want to infer that it is perfectly permissible to draw an analogy between that paradigm shift and the current one taking place, implying that ID thinkers are blinded in some way.

    If you actually read the comments I linked to, you’d find….

    Now that we actually have two theories – one explicit and on implicit – was there a way we could have differentiated between them at the time? I’m going to suggest that [A] there is such a thing as a bad explanation and [B] there really are ways we can identifying them.

    [...]


    Again, as a critical rationalist, I realize intuition, observations and induction are insufficient on their own as any theory can make any prediction. Ultimately, It’s the arguments and explanations behind them which makes one tenable over another.

    […]

    In other words, to understand planetary motions via the Inquisition’s implied theory it’s essential to reference Heliocentrism. It’s a cosmology that can be only understood in terms of a different cosmology which it contradicts but faithfully mimics. The result is that Inquisition’s theory does not actually explain planetary motion without having to introduce the complication of Heliocentrism first. As such, we can rightfully say that the Inquisition’s implied theory is a convoluted elaboration of Heliocentrism.

    […]

    In case it’s not clear, I’m suggesting that we can rightfully say ID’s implied theory is a convoluted elaboration of and a response to TOE. Furthermore, it shares the following with The Inquisition’s implied theory and even Solipsism: it draws an arbitrary boundary beyond which human reason and understanding has no access and problem solving can no longer increase knowledge.

  54. veilsofmaya (#50 – 51):

    1) First of all, the lungfish (and other similar giant genomes). The C enigma is, as far as I know, still an enigma. If you are aware of recent literature which has detailed in some way the composition of the lungfish genome (or of any other giant genome), I will be very grateful if you can point that to me.

    I have found this paper of 2005:

    “NfCR1, the first non-LTR retrotransposon characterized in the Australian lungfish genome, Neoceratodus forsteri, shows similarities to CR1-like elements”

    which analyzes a retrotransposon in the lungfish genome, and finds it to be account for 0.05% of the genome (the same % as in chicken). That’s interesting, but is really too little.

    Beware, I am not underestimating the importance of these giant genomes. Though they are certainly more an exception than the rule, they can probably give us important insights about some unsolved problems (and, in general, help us understand better the C enigma). I have been waiting for years to know more about those genomes.

    But my point is, until we know something substantial about those genomes, and their structure, we cannot even begin to discuss why they are so big. So, I don’t think you can use them as evidence of any sort of principle in any discussion about the functions of DNA, be it coding or non coding.

    2) About your other remarks, I would say that I am drawing no arbitrary boundary. The difference between harmful traits and useful new functions is extremely objective, and Behe has discussed that in great detail in TEOE: harmful tracts are simple, new functions are complex.

    Take, for instance, mendelian genetic diseases: they are ususally due to a single point mutation, which reduces or abolishes some important protein function. we all agree (darwinists and IDists) that random single point mutations do occur. That they are frequent. Living cells have a whole set of complex functions to try to deal with negative simple mutations. I would not even agree to call them “unplanned errors on the part of nature”, because nature, if considered blind, does not make errors: it just proceeds through unmeaningful events.

    The thing is very different for complex functions. Functional proteins are both specified and complex. They cannot emerge form random noise, not even with the help of necessary NS. That’s the whole point of ID.

    So, I am drawing no arbitrary boundary, except for the very natural and logical one between what is complex and what is simple, what specifies a completely new function, and what simply and accidentally destroys an existing one.

    A very simple example can show the difference. Sometimes darwinists discuss experimental models where bacteria undergoe a mutation, usually induced by the researcher, which inactivates a protein. In those cases, in the appropriate context, microevolution can, with some relative ease, reintegrate the previous function through random mutation.

    Now, some darwinists argue: isn’t that evidence that CSI can be acquired through one simple mutation, and therefore it is not complex? After all, the non functional protein changes to the functional one through one single mutation.

    Bit it’s obvious that that’s not the case. The non fucntional protein still keeps the whole functional structure except for one aminoacid which has been accidentally changed. From that position, it is obvious that it is relatively easy to go back to the full functional structure by one appropriate substitution, which is perfectly in the reach of the probabilistic resources of a bacterial model.

    But, if the harmful mutations are two, we can already see that the difficulties increase exponentially. Indeed, two coordinated mutations are almost a natural boundary which is traversed very rarely and only through huge probabilistic resources, as shown by Behe. If they are not the edge of unguided evolution, they are very near. And three mutations? Four? Five?

    Please consider that basic protein domains differ one from the other for tens, up to hundreds, of AAs. That’s the boundary. It’s not me who am drawing it. It’s reality itself.

  55. bornagain77 (#46):

    Thank you for the link to the interesting paper: I am looking at it.

  56. “There is now considerable evidence that genes alone do not control development. For example when an egg’s genes (DNA) are removed and replaced with genes (DNA) from another type of animal, development follows the pattern of the original egg until the embryo dies from lack of the right proteins. (The rare exceptions to this rule involve animals that could normally mate to produce hybrids.)

    When a similar experiment is done in plants, the results refute Wells et al. in no uncertain terms.

    Then there is the fact that single, isolated plant cells that have a completely deprogrammed cytoskeleton and have been removed from all maternal influence can grow into normal, fertile plants. Another fact that flies in the face of the mistaken claims of IDists that there is some mysterious, ethereal factor or force that plays roles in multicellular development.

  57. Re: gpuccio @ #45

    I think it needs to be pointed out that the sort of duplication event that yields pseudogenes such as PTENP1 does not involve merely the protein-coding sequence; all of the gene, including promoter, 3’ UTR, and miRNA target site (the decoy site in the pseudogene-encoded RNA) come from the original gene, and they are all duplicated.

    And, as I have stated before, and as countless ID proponents have insisted every time they are asked about gene duplication as it relates to the origins of new proteins, the ID party line is that this is not a change in information.

    Thus, when you say:

    My point is, if we believe that transcription and translation of the original gene are finely regulated by a complex network, including miRNAs (and many other regulatory modalities), then the duplication-mutation event must be finely tonuse to integrate in such a network. The point is not that the event in itself is “possible” through known random biochemical mechanisms. It certainly is, exactly as the mutations which can bring to a new functional protein are certainly “possible” from a biochemical point of view.

    you seem to miss the simple point that the duplicate gene will automatically be “finely tuned” to co-express with the original gene. It’s unavoidable, and a natural consequence of the random duplication event.

    The ID point is that such events are rare functional examples among a huge majority of non functional possible events.

    I don’t believe you have any data to support the ID position that such events are so impossibly rare as to be beyond the bounds of normal evolutionary processes. Indeed, the deep sequencing that is being done in humans reveals just the opposite – that all manner of genetic alterations, such as deletions and duplications, are not impossibly rare.

    The ID point is that, exactly as obtaining a new functional protein is empirically impossible through RV and NS alone,

    This ID point is clearly not correct.

    in the same way obtaining a finely tuned duplication, or set of duplications, and the coordinated mutations both in the coding and non coding sequence and in the related regulatory sequences, which perfectly integrates in a complex regulatory system involving many different agents, is empirically impossible through RV and NS alone.

    The problem is that, in the case under discussion here, all of this fine tuning is an unavoidable consequence of a single random event.

    We have no evidence that those “typical biochemical processes” are random and unguided, any more than we have evidence that all single point mutations are random and unguided.

    We know that all of these processes involve well-understood chemical rules, and that no “hand of God” (with all apologies to football fans, and especially those aggrieved by the alluded-to event) need be invoked to understand the past, present, or future when it comes to gene duplication.

    If you have positive, repeatable and controlled experimental data that suggests otherwise, please discuss it. Until then, the suggestion that something other than chemistry is behind gene duplication must be considered as idle fancy.

    Moreover, many pseudogenes are the result of transposon activity, and transposon activity is a very good candidate as an interface for guided variation.

    The pseudogenes of interest here have nothing to do with transposons (which are not guided in any ways, other than the substrate preferences, as determined by chemistry, of the enzymes that catalyze transposon duplication and movement).

    To reiterate, we are talking about something here that is at best information-neutral, and at worst involves a loss of information. And it is the result of a common and random process.

  58. Another fact that flies in the face of the mistaken claims of IDists that there is some mysterious, ethereal factor or force that plays roles in multicellular development.

    I know of no IDist of any repute who makes that claim for the devlopment (as in cell to mature individual) of organisms in existence today. Development follows a developmental program.

    Multicellar evolution (as in when the first unicellular organism became multicellular) is different from multicelluar development.

    I invite the readers to do a google search to see how many times the phrases: “intelligent design” and “multicellular develpment” and “ethereal force” come up together. :-)

  59. veilsofmaya [52 and 53]:

    Try to be more clear about what you’re saying. For example, what is this supposed to mean?

    As such, wouldn’t this be a “very bad day” for those who continually, perpetuate, these claims, despite research such as this which clearly suggests otherwise?


    You seem to be suggesting that IDists are the one suggesting that there is no function to junk DNA, which is, of course, quite the opposite. So who are these people who “continually, perpetuate, these claims”? And why is there a comma between continually and perpetuate, and one following perpetuate?

    I shouldn’t be expected to make sense out of all of this.

    And, as to #53 and this quote:

    it draws an arbitrary boundary beyond which human reason and understanding has no access and problem solving can no longer increase knowledge.

    I’ll presume you’re the author of this quote. Can’t you see that this applies exactly to neo-Darwinists who continually state: “Well, who is this Designer? We know what humans are capable of, but we don’t know anything about this Designer. So how can we possibly detect his design.”

    Doesn’t this exactly draw “an arbitrary boundary beyond which human reason and understanding has no access and problem solving can no longer increase knowledge.”

    When you start pointing fingers, you ought to be careful.

  60. Art, why don’t you provide a link to your final claim in #56?

  61. When a similar experiment is done in plants, the results refute Wells et al. in no uncertain terms.

    But plants are not animals, and that could be a hasty extrapolation. Replacement of some genes in some plants does not necessarily result in observing ill effect, but we can’t extrapolate that to all plants and animals in all reasonable contexts.

    And here earlier you were objecting to making extrapolations from limited observation, and the argument you put forward does exactly that.

    But the bottom line is, do you believe “genes alone control all development” or do you believe information apart from genes is necessary to effect development, such as pseudogenes?

    I think that will help clarify the discussion. Do you beleive pseudogenes serve function in development? Do you think this would be a worthy area of research?

  62. Art, why don’t you provide a link to your final claim in #56?

    I would be interested, too.

  63. Art Hunt, I’m wondering just how much weight you should give to your link,,, for the plants seem to be related:

    Solanum, the nightshades, horsenettles and relatives, is a large and diverse genus of annual and perennial plants.
    http://en.wikipedia.org/wiki/Solanum

    Nicotiana (pronounced /?n?k??i?e?n?/)[3] is a genus of herbs and shrubs of the nightshade family (Solanaceae)
    http://en.wikipedia.org/wiki/Nicotiana

    i.e. has one descended by means of genetic entropy from the other? The reason I ask is because quite a bit a variability can be found in plants from just one parent stock:

    Evolution? – The Deception Of Unlimited Variation – video
    http://www.metacafe.com/watch/4113898

    i.e. variation within kind!

    Now Art if you put the DNA from say a dog into a cat and had a dog develop then you will have saved the DNA dogma. But as it sits I am not impressed.

  64. bornagain,

    In answer to your claim that transcription = function for noncoding dna, my friend laughed again and pointed out that there is massive evidence that most transcription of most protein encoding genes that have been studied is nonfunctional, and we know this from studying mutants, even humans.

    He defines functional as “having any detrimental effect on the organism when it is not present.”

  65. Joaozinho-

    That’s a naive definition of functional and can you please have your friend speak for himself and you speak for yourself.

  66. Can you or your friend pick a percent number for just how much Junk DNA you think is present as I asked earlier Joaozinho? as well Can you or your friend cite any studies as to declaring protein coding genes (of all things) to be junk?

  67. Art Hunt,, I’m finding the link you listed to fall within Genetic Entropy:

    Agricultural Applications of Plant Protoplast Fusion

    David A. Evans1
    Abstract

    Plant protoplasts can be fused and the fusion products cultured to produce somatic hybrid plants. This technique has been used to produce germplasm previously unavailable to the plant breeder. Several researchers have emphasized production of hybrids between distantly related, sexually incompatible species, but many of these hybrids are sterile, precluding incorporation into a breeding program. Hence, to transfer traits such as disease and herbicide resistance, emphasis has shifted to production of hybrids between more closely related species. Novel variation has been observed in such somatic hybrids due to segregation of mixed organelles, cytoplasmic and nuclear gene recombination, and somaclonal variation. The unique gene combinations made possible by protoplast fusion ensure that new plant varieties will soon be derived from somatic hybridization.
    http://www.nature.com/nbt/jour.....3-253.html

    Do you disagree with that assessment Art Hunt?

  68. 1. One report (of hundreds or thousands) that describe the regeneration of normal plants from isolated somatic cells.

    2. The cybrid example is one that shows that, contrary to the claims of Wells et al., the nuclear DNA does indeed determine form. It’s entirely consistent with, oh, a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis.

    ID proponents need to give up on this failed assertion – it only leads to very puzzling claims (such as some of the suggestions about plants and animals that we are seeing here). Facts are facts – there is an exorable and unbreakable link between “the DNA” and multicellular growth and development, a link that is positively affirmed in systems that are amenable to appropriate experimental study.

    3. “Genetic entropy” as laid out in Sanford’s book is a concept that is utterly irrelevant to this discussion, as well as biology in general. And it most certainly does not apply to the example I gave that refutes Wells et al. in no uncertain terms.

  69. Phaedros,
    In what way is the definition naive?

    bornagain,
    Where did you get the idea that because most of the transcription is nonfunctional, that anyone’s declaring anything to be junk?

    This has been a real education for me…gpuccio admitted that PaV’s post wasn’t accurate, but when I contrast what my friend says with what the rest of you are saying, my friend has a lot more credibility. He points me to evidence, while you point me to what people say about the evidence.

  70. veilsofmaya,

    Sorry for the late reply, sometimes it takes me a few days before I can come back. Anyway, here is the full New Scientist quote:

    Myth: Junk DNA is not junk after all

    Once the vast majority of our DNA was dismissed as junk, but now we know it is important – or so you might have read recently. In fact, it still appears likely that 85 to 95 per cent of our DNA is indeed useless. While many bits of DNA that do not code for proteins are turning out to have some function or other, this was predicted by some all along, and the overall proportion of our DNA with a proven function remains tiny.

    You wrote @49:

    Darwinsts clearly do not claim that “DNA is junk”

    and also:

    Again, they do not suggest it is “useless” in it is universally non-functional. Nor do they suggest we may not find other functions for non-coding DNA. You seem to be conflating the class of junk DNA with universal non-function.

    Let’s talk about nothing but the plain reading of the NS article. I think that title implies that junk DNA is indeed junk. Later it says that it is “likely … indeed useless”. Putting everything together, this article does not orientate the reader to do more research into unknown functionality. Instead, it makes a statement that 85 to 95 percent of our DNA is useless. The solid opinion of the author is clear from the title. Nevereless, later it uses the word “likely” to provide an exit clause.

    Does this article seem to be conflating the class of junk DNA with universal non-function? :)

    To me it seems highly unlikely that such gross inefficiency was at the base of life. Especially because living creatures can vastly outperform our best technology, like the humble fruit fly. We have never created autonomous flying vehicles with optical, mechanical and chemical sensors that can seek out various targets, avoid dangers and re-fuel when needed. The fruit fly does in in a few cubic mm of volume. I bet my money that we will find function for the vast majority of DNA. For me, the context implies it so.

  71. Joaozinho:

    Just to be precise:

    gpuccio admitted that PaV’s post wasn’t accurate

    What I wrote is what I wrote, and can be read by anyone. The above statement is your statement, and not mine.

    You know, that’s just to remind you that I am not “your friend”, and that I can speak for myself if I want.

  72. Art Hunt,

    In order to support this “dated” assertion with full integrity,,,

    “a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis.”

    ,,,,You must also address the more recent evidence presented for cortical inheritance, i.e.,, live memory, instead of just presenting very interesting experiments done exchanging genetic material between closely related sub-species:

    Cortical Inheritance: The Crushing Critique Against Genetic Reductionism – Arthur Jones – video
    http://www.metacafe.com/watch/4187488

    “Live memory” of the cell, the other hereditary memory of living systems – 2005
    Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory.
    http://www.sciencedirect.com/s.....3daa6bdef8

    I am not saying DNA does not have a very important role in form and function, I am just saying that you are completely missing the point that DNA is, by far, not the whole story for form and function! Which is exactly the main point that Wells and company make!

    as a side note Art Hunt,, Dr. Sanford is the one who developed the “gene gun” that is a major technique that is used to exchange genetic material between closely related plants in the first place, even “before” he wrote his book on Genetic Entropy, so do you think that he just might have noticed if your examples went against the overriding principle for biology he established in his book?

  73. 73

    Joaozinho,

    Did you say you’re a religious studies major? Who is this “friend” of yours? A friend from Stanford?

  74. Joaozinho, though you and “your friend” may laugh at this following paper as well, I find it very indicative of the great divide as to how IDists approach the genome and how evolutionists approach it:

    Human Genome “Infinitely More Complex” Than Expected – April 2010
    Excerpt: Hayden acknowledged that the “junk DNA” paradigm has been blown to smithereens. “Just one decade of post-genome biology has exploded that view,” she said, speaking of the gene regulation was a straightforward, linear process of gene coding for regulator protein that controls transcription. “Biology’s new glimpse at a universe of non-coding DNA – what used to be called ‘junk’ DNA – has been fascinating and befuddling.” If it’s junk, why would the human body decode 74% to 93& of it? The plethora of small RNAs produced by these non-coding regions, and how they interact with each other and with DNA, was completely unexpected when the project began.,,, In the heady post-genome years, systems biologists started a long list of projects built on this strategy, attempting to model pieces of biology such as the yeast cell, E. coli, the liver and even the ‘virtual human’. So far, all these attempts have run up against the same roadblock: there is no way to gather all the relevant data about each interaction included in the model.,,, The p53 network she spoke of is a good example of unexpected complexity. Discovered in 1979, the p53 protein was first thought to be a cancer promoter, then a cancer suppressor. “Few proteins have been studied more than p53,” she said. “…Yet the p53 story has turned out to be immensely more complex than it seemed at first.” She gave some details: “Researchers now know that p53 binds to thousands of sites in DNA, and some of these sites are thousands of base pairs away from any genes. It influences cell growth, death and structure and DNA repair. It also binds to numerous other proteins, which can modify its activity, and these protein–protein interactions can be tuned by the addition of chemical modifiers, such as phosphates and methyl groups. Through a process known as alternative splicing, p53 can take nine different forms, each of which has its own activities and chemical modifiers. Biologists are now realizing that p53 is also involved in processes beyond cancer, such as fertility and very early embryonic development. In fact, it seems willfully ignorant to try to understand p53 on its own. Instead, biologists have shifted to studying the p53 network, as depicted in cartoons containing boxes, circles and arrows meant to symbolize its maze of interactions.
    Network theory is now a new paradigm that has replaced the one-way linear diagram of gene to RNA to protein. That used to be called the “Central Dogma” of genetics. Now, everything is seen to be dynamic, with promoters and blockers and interactomes, feedback loops, feed-forward processes, and “bafflingly complex signal-transduction pathways.”
    http://www.creationsafaris.com.....#20100405a

    as well Joaozinho, I noticed you nor “your friend” have picked a number for Junk DNA yet.

  75. Joaozinho,

    Your friend says that my claims are exaggerated. Gpuccio has defended my position, and the ID position, admirably. I agree with every point he makes, and would have made the same points myself (although not quite as nicely).

    I’m reminded of what is said of Winston Churchill. (I could very easily be wrong about it being Churchill) It is said that he once got into a discussion with a woman who made the comment that no amount of money would get her to sleep with another man. He asked her if she would sleep with him for a million dollars. She said, “Well, for a million dollars, yes.” Then he asked her if she would sleep with him for 50 dollars. She said to him, “What kind of a woman do you think I am?” He answered that he already knew what kind of a woman she was, and that they were simply haggling over the price.

    Even if, right now, the amount of pseudogenes that have function is small (per A Hunt’s calculation), neo-Darwinian theory is nevertheless under duress since even a 23 bp miRNA doesn’t just happen by chance—which is exactly the neo-Darwinian understanding of how gene duplication + RM(=neutral drift) + NS = a new, “coding” gene. Did the 23 bp regulatory function come about by chance? (The odds are 1 in about 10^14; ie, 1 in 100 trillion) Not only that, if the pseudogene has a function while being transcribed, though not translated into a protein, then the translation process would likely lead to a loss of the miRNA function. And, if the miRNA, small as it may be, is involved in gene regulation, that could easily have catastrophic effects for the organism.

    You have heard of the proverbial “tip of the iceberg,” well, this finding, most likely, is just that. It represents a severe blow to Darwinian story telling. But, of course, the Darwinists don’t see it that way.

  76. PaV (75),

    I think it was George Bernard Shaw.

    The thing that gets me about this junk DNA business is: if there’s a view that it isn’t junk then why isn’t the Biologic Institute looking at it as a research project? It should be a fertile research area if it isn;t really junk.

  77. why isn’t the Biologic Institute looking at it as a research project?

    Where have I heard that question several times before??? My My,,, I think Nakashima has a twin.

  78. 78

    Joaozinho,

    This has been a real education for me…gpuccio admitted that PaV’s post wasn’t accurate, but when I contrast what my friend says with what the rest of you are saying, my friend has a lot more credibility. He points me to evidence, while you point me to what people say about the evidence.

    And you don’t point to what your “friend” says about the evidence? The only way that your statement above doesn’t also lose credibility for you in the same way that you begrudge others, is if there is no “friend”, in which case you would lose credibility too. It looks like a no-win situation for you Jo(aozinho)hn.

  79. 79

    bornagain77,

    Where have I heard that question several times before??? My My,,, I think Nakashima has a twin.

    Neither one of them actually know what the Biologic Institute is or isn’t looking at as a research project.

  80. Clive:

    “And you don’t point to what your “friend” says about the evidence?”

    Yes, but I also get actual evidence. For example, gpuccio says, “That’s [what proportion of genes are transcribed is] absolutely not known.”

    Then I get this manuscript and others:
    http://papers.gersteinlab.org/.....eprint.pdf

    And then what absolutely happens to gpuccio’s credibility?

  81. 81

    Jo(aozinho)hn,

    And then what absolutely happens to gpuccio’s credibility?

    It’s the same as yours as far as pointing to what others say. Having a manuscript doesn’t mean that you’re not pointing to something someone else said. Anyone can point to a manuscript. You just did, and gpuccio certainly can. But it should be remembered that the mere pointing to others is what loses one credibility, according to you. Did you write that manuscript, or are you pointing to what another person said? If you are pointing to what another said, you lose credibility in the same way you claim others do. Are you going to argue the merits of the argument at hand or keep making red herring arguments about credibility that are self-referentially damaging?

  82. bornagain77 (77) and Clive Hayden (79),

    Okay – are they doing the work or not? If not, maybe they should be.

  83. 1. One report (of hundreds or thousands) that describe the regeneration of normal plants from isolated somatic cells.

    I think it inappropriate to generalize the development of plants to animals and humans and things like Dolly the Sheep. :-)

    I don’t know many embryologists who would think what you see happen in tobacco will happen in a live human being or even a clonable sheep.

    The experiment you cited discussed tobacco cells put in agar and then growing. I’d expect you wouldn’t want to be arguing that such a thing will happen for humans, but that is exactly your inference. It is unwarranted extrapolation.

    Wells focuses on animal embryology, not plant embryology. Thus your supposed counter examples are suspect.

    Epigenetic Developmental plasticity is in Mary Jane West Ebberhard’s book. Her work lists counter examples to your generalization that what happens in certain nuclear DNA of plants must necessarily be generalized to animals!

    2. The cybrid example is one that shows that, contrary to the claims of Wells et al., the nuclear DNA does indeed determine form. It’s entirely consistent with, oh, a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis.

    Wells never said there is no genetic basis, that is your misrepresentation. You’re welcome of course to provide citations where Wells said: “there is no genetic basis for form”.

    I recall some of us have requested citations to support your other misrepresentations of ID proponents, like “ethereal force” that ID proponents somehow invoke to explain development.

    So the request remains:

    1. citation for “ethereal force” that is involved in animal development

    2. citation where Wells says there is no genetic basis for form

    PS
    Wells cites hox genes in the Icons Video invovled in form, so Wells does claim genetic involvement in form. Art’s misrepresentation is just that, a misrepresentation.

    I appreciate Art’s valor and determination to oppose us, and I appreciate his visits and participation. But if attributes arguments to ID proponents which they’ve never made, I feel a bit compelled to speak up.

    Art may think that’s what he heard them say. He may think that’s what they mean. But let’s clarify what they really said versus what he thinks they said.

  84. Clive,
    “It’s the same as yours as far as pointing to what others say.”

    But what about as far as pointing out what is or isn’t known, Clive?

    “Having a manuscript doesn’t mean that you’re not pointing to something someone else said.”

    I’m pointing to what they did.

    “Anyone can point to a manuscript. You just did, and gpuccio certainly can. But it should be remembered that the mere pointing to others is what loses one credibility, according to you. Did you write that manuscript, or are you pointing to what another person said?”

    What they did, more specifically, what is known about pseudogenes.

    “If you are pointing to what another said, you lose credibility in the same way you claim others do.”

    I’m pointing to what they did.

    “Are you going to argue the merits of the argument at hand …”

    I’m not sure what that means.

    I’ll go with evidence. When I do go with what someone says (and we all have to do that in many cases), it’ll be based on how much evidence is offered with the rhetoric.

    “Neither one of them actually know what the Biologic Institute is or isn’t looking at as a research project.”

    Wouldn’t looking at the Biologic Institute’s IRS Form 990 to see what they’ve purchased give us a general idea?

  85. 85

    Being disingenuous is typically grounds for the loss of credibility. I’ve never noticed GP being disingenuous, in fact, the opposite is his unsolicited trademark.

  86. scordova,

    When you asked Art for a reference for someone alluding to a “ethereal” force in body formation,,,,,, actually I, though many of my opinions are certainly not highly regarded nor shared by others, have argued for a more direct role for God in “conducting” the formation of humans: Primarily because of this:

    Jeremiah 1:5
    Before I formed you in the womb I knew you, before you were born I set you apart;
    http://www.uncommondescent.com.....ent-338098

    basically I tried to defend that position from a Quantum Mechanic/4D space-time angle plus from the fact that no one really knows for sure where the complete set of ontogenetic information resides for body formation. I don’t think I convinced many people, and empirical validation would seem to only be possible through total elimination of all other possibilities, but none the less, I still am fairly confident that God will be found to have some “orchestrating” role in body formation however long it takes to “prove” it.

  87. Contrary to Art’s misrepresentation of Wells, here is an example that shows that Wells accepts that there is a genetic basis for form:

    Hox genes, which affect the character of body segments during embryo development. For example, a mutation in one Hox gene can cause a fruit fly to sprout a leg from its head in place of an antenna. Remarkably, vertebrates possess Hox genes that are very similar to a fruit fly’s, so similar that a mouse Hox gene can enable normal development in a fly embryo that lacks its corresponding Hox gene

    Uncommon Descent: Jonathan Wells on the contemporary state of Evo-Devo

    I think a retraction of this misrepresentation by Art is in order:

    the claims of Wells et al., the nuclear DNA does indeed determine form. It’s entirely consistent with, oh, a hundred years or more of genetic and molecular analysis that shows that form and function in all living organisms has a genetic basis.

  88. Even if, right now, the amount of pseudogenes that have function is small (per A Hunt’s calculation), neo-Darwinian theory is nevertheless under duress since even a 23 bp miRNA doesn’t just happen by chance—which is exactly the neo-Darwinian understanding of how gene duplication + RM(=neutral drift) + NS = a new, “coding” gene. Did the 23 bp regulatory function come about by chance?

    PaV, you may have missed the back-and-forth with gpuccio, so I’ll repeat the bottom line – the probability that the expressed pseudogenes will have the microRNA target is exactly 1. This is because the same microRNA target that is in the progenitor gene gets duplicated, along with everything else.

    That having been said, your estimates of the “probability” of origination of microRNA targets is quite wrong. I explain why here.

    One aside – a comment Wells made directly to me several years ago on another board:

    [Art] seems to have missed my main point, which I will re-state: whatever is controlling development and morphology (and is thus the key to evolution), it is NOT the genes (Hox or any others).

    Here’s why:

    1) The cells in a multicellular animal are radically different from each other in structure and function, yet virtually all of them contain the same DNA; therefore, whatever is making them different must be something other than their DNA.

    2) The animal phyla are radically different from each other in body plans, adaptations and life histories, yet they all contain similar homeobox genes (of which Hox genes are one kind); therefore, whatever is making them different from each other must be something other than their homeobox genes.

    Substitute “hox genes” with “DNA” and you can see where I get my (accurate) estimations of the assertions of IDists.

  89. Arthur Hunt (#57):

    I think it needs to be pointed out that the sort of duplication event that yields pseudogenes such as PTENP1 does not involve merely the protein-coding sequence; all of the gene, including promoter, 3’ UTR, and miRNA target site (the decoy site in the pseudogene-encoded RNA) come from the original gene, and they are all duplicated.

    To be more precise, according to the paper:

    “PTENP1 is a processed pseudogene located at 9p13.3; it is highly
    homologous to PTEN, with only 18 mismatches throughout the coding sequence. A missense mutation of the initiator methionine codon prevents translation12. PTENP1 possesses a 39 UTR that is 1 kilobase shorter than that of PTEN (Fig. 1b). It can be divided into two regions relative to its homology with the PTEN 39 UTR: a
    high homology (95%) 5′ region and a low homology (50%) 3′ region (Fig. 1b and Supplementary Fig. 1). Within the high homology region, we found perfectly conserved seed matches for the PTEN targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families”

    That’s not exactly the picture of a complete passive duplication, but of duplication with many specific variations.

    you seem to miss the simple point that the duplicate gene will automatically be “finely tuned” to co-express with the original gene. It’s unavoidable, and a natural consequence of the random duplication event.

    I don’t agree. The key point here is that the duplicated gene is not only “co-expressing” with the original gene. It is regulating its expression. That’s a completely different concept.

    IOW, simple random co-expression of an already regulated gene cna probably only interfere with the fuin ction of that gene system. Here, instead, what we observe is that the regulatory function of the duplicated gene is essential to the function of the existing gene, so much so that, according to the authors, it has a tumour suppressive role. That’s what I mean with “fine tuning”. A mere duplication with co-expression, with or without translation, is not fine-tuned at all. Fine tuning implies that the whole system (gene + duplicated gene) exhibits a perfect functional equilibrium.

    I don’t believe you have any data to support the ID position that such events are so impossibly rare as to be beyond the bounds of normal evolutionary processes. Indeed, the deep sequencing that is being done in humans reveals just the opposite – that all manner of genetic alterations, such as deletions and duplications, are not impossibly rare.

    Again, I think you misunderstand. The ID position is certainly not that deletions and duplications and all other kinds of genetic alterations are rare. The ID position is that, if they are truly random, it is not credible that they can generate complex functional results. Again, it’s completely different.

    This ID point is clearly not correct.

    I don’t understand. Again, you are not demonstrating in any way that the molecular events you are pointing to could generate function through a random search. I will go back to the essential: single point mutations. Not because they are the only mechanism, but because what is true for them is true for all random variations. I am not saying that single point mutations don’t happen (that would be very silly). I am just saying that purely random single point mutations cannoy build a new protein domain. But designed mutations certainly can. The same is true for all kinds of genetic variation. RV cannot generate complex function, while designed variation certainly can.

    This is the ID point. To show that it is wrong, you don’t have to just say that variation happens in different ways, and that different types of variation can be responsible of the origin of different types of genes. I agree on that. You have to credibly demonstrate that those variations are in the reach of random events, even with the help of NS, if and where that help can be credibly incorporated in the model.

    The problem is that, in the case under discussion here, all of this fine tuning is an unavoidable consequence of a single random event.

    As I have argued above, that’s not true. A single random event of duplication would only bring non functional, or probably harmful, competition. Fine tuned regulation is all another thing.

    We know that all of these processes involve well-understood chemical rules, and that no “hand of God” (with all apologies to football fans, and especially those aggrieved by the alluded-to event) need be invoked to understand the past, present, or future when it comes to gene duplication.

    The argument about chemical rules is really old and poor. There is no reason to break chemical rules to design a protein. Protein engineering is all about designing proteins, and I don’t thing protein engineering breaks any chemical rule. And still it is a designed process. Information is intelligently guiding the process, without violating any chemical rule.
    How is it possible that darwininsts miss so easily the difference between deterministic laws at low level, and the supervening informational order at higher level? And yet it is not a complex concept. Do you really believe that software is not designed, because processors and hard disks and RAM do not break any physical law? I would definitely say that, to have complex functional software, a “hand-of-designer” is badly needed.

    If you have positive, repeatable and controlled experimental data that suggests otherwise, please discuss it. Until then, the suggestion that something other than chemistry is behind gene duplication must be considered as idle fancy.

    Again, the suggestion is that something other than chemistry is behind functional, tweaked and finely tuned gene duplication which implements a very successful regulation.

    The pseudogenes of interest here have nothing to do with transposons (which are not guided in any ways, other than the substrate preferences, as determined by chemistry, of the enzymes that catalyze transposon duplication and movement).

    From the paper:

    “Pseudogenes exist as either processed or non-processed genetic
    elements. Although non-processed pseudogenes arose from genetic
    duplications, processed pseudogenes were generated through retrotransposition”

    and:

    “PTENP1 is a processed pseudogene”

    Did I miss something?

    And is your certainty that the activity of retrotransposons is determined only by chemistry, and cannot be guided by design, on the same level as the certainty that the assemblage of software is determined only by the electromagnetic force? Will protein engineers always be denied the chance to use transposons in their procedures, only because you don’t like the idea?

    To reiterate, we are talking about something here that is at best information-neutral, and at worst involves a loss of information. And it is the result of a common and random process.

    You are only reiterating a false reasoning.

  90. joazihno:

    (2007) Genome Res 17: 839-51

    Pseudogenes in the ENCODE Regions: Consensus Annotation, Analysis of Transcription and Evolution:

    “We believe that the data obtained by RACE experiments or by sequencing analyses (CAGE, PET, EST, and mRNA) provide unambiguous evidence for pseudogene transcription. Altogether, these data indicate that 38 (19% of 201, 20 non-processed and 18 processed) pseudogenes are the sources of novel RNA transcripts. This may well represent a low-bound estimate and does not include the ambiguous and possibly inconclusive cases supported only by transfrags.”

    Emphasis mine.

  91. me:
    “He laughed at it and said that only a tiny bit of junk dna is pseudogenes, only a minority of pseudogenes are expressed as rna…

    gpuccio:
    That’s absolutely not known.

    Emphasis mine.

    19% is a minority, is it not?

  92. Joaozinho:

    Can you understand what “a low bound estimate” means?

  93. 93

    What is not clear to me why this is a bad day for “Darwinism”. As far as I know the ToE does not predict that pseudogenes can’t have a function or generally that “junk DNA” can’t be found to have a function. Is it thus just a bad day for “Darwinism” because it is a god day for ID?

  94. second opinion:

    Is it thus just a bad day for “Darwinism” because it is a god day for ID?

    I don’t know: darwinists seem to rejoy so much for our troubles, maybe they can suffer a bit for our joys :)

  95. The ENCODE project found “conserved” regions in pseudogenes. The idea is that:

    “conserved regions” = “functional DNA”

    The unstated implication of such a Darwinist view is that

    “unconserved regions” = “non-functional DNA”

    But I disagree with that.

    In contrast to the Darwinist view, let me offer my speculation inspired by Dembski’s Steganography hypothesis:

    “conserved regions” = “functional the same way”

    and

    “conserved regions” = “functional differently”

    Thus the ENCODE methods could understate functionality.

    It should be noted that the “conserved” regions are hierarchically organized. This represents a problem. Say a feature is only “conserved” among primates in one way, and “conserved” among birds another way.

    Does that mean the primate conservation is non-functional or the avian conservation is non functional since relative to each other these regions are “non-conserved”. No, it suggests they function differently. And species specific “conservation’ (intra species “conservation”, or monomorphism) may indicate unique functionality to a species.

    The hierchical structure of “conserved” regions screams “steganography” optimized for scientific discovery.

    Single Nucleotide polymorphism may signify permitted variation or dysfunction. There is too much we don’t know.

    The point is the ENCODE methodology is reasonable to identify lots of common functions, but may understate the level of functionality since it may exclude uncommon function.

  96. TYPO:

    “NON-conserved regions” = “functional differently”

    Sorry!

  97. gpuccio: Can you understand what “a low bound estimate” means?

    Yes, and I understand what “MAY be a low bound estimate” and “that’s ABSOLUTELY not known” mean as well.

    I’m still trying to understand how the particular mechanism described in the Nature paper is thought to be more likely to have been produced by ID than by evolution.

    Can you explain that to me? Because it’s clear that the authors of the paper don’t agree with your interpretation of their data, and no one here AFAIK has attempted a step by step interpretation of the data from the paper. This seems odd given that you are clearly claiming to understand the data better than the authors do.

    I’m just not seeing how the demonstration that ~20 of ~2 billion bases of DNA has a function represents a bad day for Darwinism.

  98. Joaozinho:

    Of all people, you are not the one I am most interested to discuss with. That, just to be frank.

    But you can always look at my ongoing discussion with Arthur Hunt and, if you like, comment on that.

    Or just ask your friend to do that.

  99. scordova:

    You say that darwinists argue that:

    “unconserved regions” = “non-functional DNA”

    but that’s not always true. We have the important example of HARs, to see that, even to darwinists, that is not an universal principle. So, that would appears as:

    “unconserved conserved regions” = “super-functional DNA”

  100. Joaozinho:

    From the cheekiness of your comments on this thread, I rather suspect that you have misrepresented yourself here. I find it hard to believe that you’re a religion studies major. I think you’re simply a Darwnist in sheep’s clothing. If this is true, you should admit to it.

    Now, you say:

    I’m still trying to understand how the particular mechanism described in the Nature paper is thought to be more likely to have been produced by ID than by evolution.

    Two things: (1) ID doesn’t “produce” anything. ID provides an explanation for known and discovered biological complexity, and (2) “evolution” doesn’t produce anything either. Evolution is a fact. That is, looking at the fossil record, it is obvious that life forms have changed and grown in complexity over time. Darwinism seeks to provide a mechanism for this change and growth in complexity (i.e., the “appearance of design”). ID posits that only “agency” (a Designer) can explain the observed historical changes of form and sophisticated complexity.

    Can you explain that to me? . . . no one here AFAIK has attempted a step by step interpretation of the data from the paper. This seems odd given that you are clearly claiming to understand the data better than the authors do.

    What’s to explain? They found a functional role for parts of a transcribed psuedogene. And the pseudogene’s miRNA is involved in regulatory behavior. This is perfectly consistent with what IDists have been PREDICTING; likewise, it is in contradiction to neo-Darwinist claims that pseudogenes are no more than duplicated genes that have, through neutral drift, moved along towards the eventual goal of fulfilling some other function. (IOW, a broken down former gene, on its way to becoming a new gene—and no more.) To have pseudogenes involved in RNA regulation undermines that claim.

    You see, it’s the Darwinists who need to ‘explain’ these results. As I stated in the original post, they cannot explain the development of the genetic code, and now, lo and behold, an RNA code is rising up alongside the DNA code. Another day, another bad day for Darwinism!!!

    I’m just not seeing how the demonstration that ~20 of ~2 billion bases of DNA has a function represents a bad day for Darwinism.

    You don’t seem to understand what the authors are implying. They’re not saying we found a functional role for 20 bp out of the cell’s 2 billion. They’re saying that when it comes to this one gene they’ve found a 23 bp portion of the transcribed RNA that has a function. But the implication is that there is a whole slew of these psuedogene miRNA’s, and further, that this then implies the presence of a regulatory RNA language, with RNA “speaking” to itself. All of that remains to be discovered down the road. But this new added layer of complexity only further strains the credulity of proposing that these highly regulated networks/languages all arose simply through chance modifications.

    Another day, another bad day for Darwinism . . . .

  101. Second Opinion:

    As far as I know the ToE does not predict that pseudogenes can’t have a function or generally that “junk DNA” can’t be found to have a function.

    You’re quite right. Now, tell me, just what exactly DOES Darwinism predict?

    It predicts that we will find lots of fossil remains prior to the Cambrian. But, of course, there are none.

    It predicts that the earth is quasi-eternal, with an extremely long geological history. But, we know that instead it is of finite duration.

    So, its only predictions turn out to be wrong, and, after the wrong predictions it has made, it makes no further predictions.

    You’re free to give us one.

  102. 102

    Jo (aozinho) hn,

    Clive,
    “It’s the same as yours as far as pointing to what others say.”

    But what about as far as pointing out what is or isn’t known, Clive?

    What about it? Do you really want to talk about pointing some more? You have two options when you claim that credibility is lost by virtue of pointing to what others say. Either you lose credibility given that you also point to what others say, or you lose credibility by lying about who are and who this “friend” is to which you point. Which do you want? I know very well who you are. You are not a religious studies major, and you have no “friend” that you’ve continually made reference to. Thus you’ve lost credibility here. Would you like me to “out” you on this blog? What religious studies are you studying at Stanford? Why not stay in Montana for that?

    I’m pointing to what they did.

    What they did, but not what they said? Are you pointing to actions or to a manuscript? I thought you said it was a manuscript, which is words on a page? Didn’t you begrudge gpuccio’s credibility by claiming that he points to what others say? Does the manuscript actually show actions, like a movie, with no words? They didn’t say anything? That would be an interesting manuscript indeed.

    I’ll go with evidence. When I do go with what someone says (and we all have to do that in many cases), it’ll be based on how much evidence is offered with the rhetoric.

    Wonderful, then let’s quit this absurd red-herring argument about credibility by virtue of pointing to manuscripts. Do you know what red herring means in relation to an argument?

    Wouldn’t looking at the Biologic Institute’s IRS Form 990 to see what they’ve purchased give us a general idea?

    It would give you series of assumptions, such as claiming that the wine I used to marinate my steak meant I was an alcoholic. You’re welcome to “know” this, it’s better name is ignorance.

  103. 103

    Jo (aozinho) hn,

    Honestly I find you astoundingly hypocritical. You come to this blog under false and deceptive pretenses and have the gall to call others not credible? And I’m supposed to believe that you’re just “seeking” the truth in your Darwinism? People like you, that I’ve encountered since I began questioning Darwinism, have again and again confirmed that I am dealing with people defending a worldview by any means possible. I used to think that scientists were completely honest and impartial, but that was when I was a naive child, I know better now, I became a man and put childish things away. If the theory cannot actually be sustained by physical evidence, any tactic will work for its defenders, including dishonesty. It’s people like you that affirm that I have correctly rejected the naive assumption of the complete objectivity and honesty of scientists, and that I have correctly rejected Darwinism which needs to rely on such dishonesty as its defenders are ready to give.

  104. PaV (101),

    “You’re quite right. Now, tell me, just what exactly DOES Darwinism predict?”

    It predicts common ancestry for life on Earth.

    “It predicts that we will find lots of fossil remains prior to the Cambrian. But, of course, there are none.”

    Actually, Darwinism didn’t predict that there would be lots of fossils prior to the Cambrian – at the time of Darwin it was thought that there weren’t any fossils before the Cambrian because they weren’t known. But Darwinism predicted that there would have been life before the Cambrian, based on the fact that fossils of multicellular organisms were found in the Cambrian so there would have been life before then even if it hadn’t been left in the fossil record. In fact since then multicellular fossils have been found in Ediacaran strata, stromatolite fossile have been found in 3.5 billion year strata (and recently multicellualr fossils from 2 billion years BP appear to have been found).

    “It predicts that the earth is quasi-eternal, with an extremely long geological history. But, we know that instead it is of finite duration.”

    Is it even possible for something to be “quasi-eternal”? But in any case, Darwinism certainly doesn’t predict an eternal earth, just an age of earth long enough for life to evolve.

  105. Art:

    And, as I have stated before, and as countless ID proponents have insisted every time they are asked about gene duplication as it relates to the origins of new proteins, the ID party line is that this is not a change in information.

    If you have one dictionary and I give you a copy of the same dictionary, do you have more information or just two dictioaries with the same information?

    Also you need to read “Not By Chance”- it explains gene duplications.

    you seem to miss the simple point that the duplicate gene will automatically be “finely tuned” to co-express with the original gene.

    Not without all the regulatory stuff that goes along with the expressing part.

    And even then all you are going to get is another polypeptide that can clog things up.

    We know that all of these processes involve well-understood chemical rules, and that no “hand of God” (with all apologies to football fans, and especially those aggrieved by the alluded-to event) need be invoked to understand the past, present, or future when it comes to gene duplication.

    Don’t need a programmer present to run my computer and perform spell-checks.

    You should read “Not By Chance”.

    That way you may understand the argument you are trying to “refute”.

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