Home » Intelligent Design » De Novo Genes: The Evolutionary Explanation

De Novo Genes: The Evolutionary Explanation

Cells have remarkable adaptation capabilities. They can precisely adjust which segments of the genome are copied for use in the cell. They can edit and regulate those DNA copies according to their needs. And they can even modify the DNA itself, such as with adaptive mutations, to accommodate environmental pressures. And in addition to these examples, cells can create completely new, de novo, genes in an evolutionary instant. It is yet another biological capability that reveals the scientific weakness of evolutionary theory.  Read more

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50 Responses to De Novo Genes: The Evolutionary Explanation

  1. Cornelius Hunter says:

    ‘cells can create completely new, de novo, genes in an evolutionary instant.’

    - He considers this evidence for ID.

    In an earlier thread, jerry says:

    ‘No natural process has been discovered that builds up information over time. And no observation of increased information has been observed.’

    - He considers this evidence for ID.

    Gentlemen, can you understand why I’m still confused?

  2. faded-Glory,

    I can understand your confusion, but I think I can explain.

    1. Most importantly, are the words “natural process.” I think, (correct me if I’m wrong) that Mr. Hunter is saying that there is some kind of ongoing design by an intelligent designer.

    2.Mr. Hunter has many of his own ideas and is not quite as closely associated with ID as Meyer, Dempski and Behe. His views may not conform exactly to the main Discovery Institute message that Jerry is propounding. But since his message is on-topic and he is ID-friendly, he is invited to be a contributor to the blog (is my guess).

    3. Mr. Hunter, when he says “cells create” may be speaking sarcastically or ironically or whatever the right word is. I think his argument is that it would be impossible for cells to do so without some mind causing it to happen. (whether the fungus that triggers the mutation is anticipated, or whether a new intervention has recently occurred or whether cells have minds of their own, literally; I don’t know).

  3. We may not be able to compute precisely the probability of evolution’s explanation for de novo genes such as T-urf13, but we do know the chances are not very good.

    It would seem to me that calculating such a probability doesn’t require an expensive lab to calculate, just a computer and some expertise in biology and probability. Since that seems to describe you, Dr. Hunter, I was wondering if you are working on the calculation?

  4. First of all if I make an absolute comment it is for hyperbole. So if I say

    “No natural process has been discovered that builds up information over time. And no observation of increased information has been observed.”

    It is a generally true statement but like anything that operates on a random basis, there are occasional exceptions. I am willing to allow the T-urf13 protein as an example of a random process that created a functional protein. And I would take the argument more seriously if the evolutionary biology community presented a whole series of studies of how the various proteins were built. But they have not and what we get is the occasional odd ball example when what should be presented should be a whole pattern of the processes and the origin of new genes.

    Having observed this debate for 10 years now, I can usually make a better case for naturalistic evolution than most of those who come here. I read Dawkins, Coyne, Miller, Collins and they are all deficient and that is the A Team. So even the best don’t seem to be able to justify naturalistic processes as leading to anything of consequence in the evolution debate. When they do, they will be considered.

  5. Jerry,

    But your “hyperbole” might still be right. No one observed nature creating this protein via random mutation and natural selection. Frontloading could be an explanation as could continuing intervention. Also, the de novo gene could have been extant in past strains but got passed along in only a few.

  6. jerry

    I read Dawkins, Coyne, Miller, Collins and they are all deficient and that is the A Team.

    Do you really consider yourself playing in the ID A team?

  7. “But your “hyperbole” might still be right.”

    It closer to the truth than anything else. The other point of view requires 100% adherence to something that has rarely been shown to happen. Everything they say is actually a greater level of hyperbole.

  8. Jerry,

    But they have not and what we get is the occasional odd ball example when what should be presented should be a whole pattern of the processes and the origin of new genes.

    How about this paper for Drosophila?

    Zhou Q, G Zhang, Y Zhang, S Xu, R Zhao, Z Zhan, X Li, Y Ding, S Yang & W Wang (2008). On the origin of new genes in Drosophila. Genome Res. (online publication)
    http://www.genome.org/cgi/doi/.....076588.108.

    It discusees several of the processes behginmd new genes. In addition, it reports approximately 11.9% of the new genes in Drosophila have de novo origins from noncoding sequences (similar to the origin of T-URF13

  9. It would seem to me that calculating such a probability doesn’t require an expensive lab to calculate, just a computer and some expertise in biology and probability…

    I see such requests/arguments from time to time, but I don’t see the relevance. Do we need the exact, precise probability to know that an explanation is deficient? It seems that one can propose the most far-fetched, outlandish hypothesis, and no one can call it improbable unless they take up the task of calculating the exact odds.

    If I find ten quarters standing on edge, I’ll assume someone placed them that way. I wouldn’t conclude that they landed that way randomly until someone could tell me the odds that they didn’t. I don’t need permission from numbers to conclude the obvious.

  10. To answer ‘faded glory’s questions, and to bring you up to date on this a little bit, Arthur Hunt and I went around on this a little while back on his blog.

    From the papers I looked at during that, let us say, discussion, the bottome line seems to be that T-urf13 results when URF-13 becomes degraded; that is, it involves a “loss of function”.

    Here’s a quote I kept from a rather recent review article on male sterility in plants:

    “The plethora of evidence that mitochondrial activity plays an important role in plant reproduction provides strong support for the loss-of-function hypothesis for the mechanism of CMS. The facility with which pollen production is impaired by disturbance to mitochondrial metabolism seems to render the search for other types of mechanism superfluous.” . . .

    “Alternatively, one possible loss-of-function hypothesis is that the efficiency of mitochondrial activity is decreased by T-URF13, resulting in an incapacity of the plants to reach a threshold of ATP production required for pollen development (Levings, 1993). . . .

    “Despite the general use of the term cytoplasmic male sterility to designate the phenomenon, neither population geneticists nor breeders have ever underestimated the role of the nuclear genotype in the phenotypic expression of CMS. Population geneticists have been confronted with the presence of restorers in the populations studied, often complicating the analysis of CMS systems in natural populations (Charlesworth and Laporte, 1998; van Damme et al., 2004). . . .
    . . . In a male sterility-inducing cytoplasm, fertility may be restored by a nuclear gene in two ways. Firstly, the nuclear gene may inhibit production of the sterility protein throughout the plant, or specifically in floral organs or tissues.
    This situation is the most frequently reported, generally with a post-transcriptional effect on the male sterility gene mRNA. . . . In recent studies, attempts to identify the male sterility determinant have often been based on the assumption that the restorer genotype affect the amount, or size, of the mRNA produced from the CMS gene . . . Alternatively, the restorer gene may restore fertility by counteracting the physiological effect of the sterility gene product. This is assumed to be the case for the Rf2 of maize Texas CMS. This restorer gene was the first to be identified and encodes a mitochondrial aldehyde dehydrogenase (Cui et al., 1996; Liu et al., 2001; Moller 2001). ‘Physiological restorers’also include genes introduced into the nuclear genomes of male sterile plants to compensate for ‘loss-of-function’ mutations.”

    “[T-URF13] remains the most widely studied CMS-associated protein, at least in part because the sensitivity phenotype, a feature unique to this system, makes it possible to carry out functional analysis in microbial cells. . . .URF13 contains three membrane-spanning domains that are probably involved in pore formation and exists in an oligomeric form in CMS-T maize mitochondria and when expressed in E. coli. . . . According to one attractive hypothesis, of the gain-of-function type, a biosynthetic molecule present only in tapetal cells may interact with URF13 in a manner analogous to that used by methomyl or T-toxin, leading to pore opening and cell death (Flavell, 1974). However, no such molecule has yet been identified.

    So, to answer the question about increased information, obviously if this involves a “loss of function” , then it involves a “loss of information.”

    As to why something that happens so quickly is considered an indicator of ID, we should consider (1) Darwin insisted on “gradualism” [his theory breaks down in places otherwise], and (2) mutational forces don’t act that quickly—for example, for a nuleotide base to mutate in an eucharyotic organism requires, on average, a trillion years(it is, of course, a much shorter time for a mutation to occur at this particular nucleotide base in a population of a million such organisms.).

  11. In a designed world I would expect de novo production of genes.

    Just think of what is needed for a new gene- start codon and stop codon, some sequence of DNA that, when broken down into codons, just happens to correspond to amino acids, a recognizable binding site in the proper region upstream and any other required regulatory signals such as activators, promoters, enhancers, and repressors.

    “Not By Chance” by Dr Lee Spetner- essential reading when discussing this topic.

  12. Dr. Spetner discussing transposons:

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

    It is also worth noting that he discusses de novo production of new genes.

    The book was published in 1997.

    The point being is we shouldn’t be discussing if it happens but how can we determine if the processes responsible can really be called blindly selected chance events.

  13. Joseph, I can also recommend Dean Overton’s book, A Case Against Accident and Self-Organization.

  14. Joseph: The point being is we shouldn’t be discussing if it happens but how can we determine if the processes responsible can really be called blindly selected chance events.

    - Fine, so we agree that there are examples of new information originating in the genome. Now the challenge is to decide if this is a process of design or not. Do you have any suggestions of how to go about that?

    Also, my understanding of the word ‘random’ as used by evolutionary biologists is not in the sense of ’caused by chance’ (whatever that means anyway) but in the sense of ‘not aimed at a specific outcome’. I think this is based on observational data that such changes are part of a wider set of events, some of which are harmful, some are neutral, and some have some net benefit. The goal is to explain the entire set, not just the beneficial ones in isolation.

    fG

  15. I see such requests/arguments from time to time, but I don’t see the relevance. Do we need the exact, precise probability to know that an explanation is deficient?

    Well, I guess that depends on your definition of precise. I would think knowing the probability to 10 significant digits probably isn’t necessary. However, you probably should know the answer to a level of precision greater than “not at all.”

    It seems that one can propose the most far-fetched, outlandish hypothesis, and no one can call it improbable unless they take up the task of calculating the exact odds.

    If you are going to claim that the probability against this is so small to render it impossible, you shouldn’t be surprised when the first question is how small. And if your answer is you don’t know because you haven’t made even the most rudimentary attempt to calculate it, you shouldn’t be surprised when no one takes you seriously.

  16. tgpeeler,

    Thanks for the reference.

    I will add it to the list.

  17. faded glory,

    The “entire set of mutations” may be due to telic and non-telic mechansims.

    How did scientists determine that mutations are “not aimed at a specific outcome”?

    (Chance means they were not aimed a specific outcome- unpredictable, accidental)

    But anyway Dr Spetner discusses hgow to make a determination- directed or undirected, in “Not By Chance”.

    I posted a brief comment from him above.

  18. It is also worth noting that Dave Wisker’s referenced paper tells us that fruit flies have developed new genes and yet all that has brought is slight differences in fruit flies.

    IOW I would say that paper supports baraminology- variation within a Kind.

  19. hummus man:

    If you are going to claim that the probability against this is so small to render it impossible, you shouldn’t be surprised when the first question is how small. And if your answer is you don’t know because you haven’t made even the most rudimentary attempt to calculate it, you shouldn’t be surprised when no one takes you seriously.

    You early suggested that Dr. Hunter should calculate the odds using a computer and expertise in biology and probability. Why should anyone bother?

    First, the premise is blatantly absurd. Should someone really get busy calculating and programming every time there’s another nonsensical theory that some complex component or feature miraculously invented itself. Such ideas merit pointing and laughing, not serious responses. (But that’s the current state of science. Oh well.)

    Second, when the most optimistic odds possible are calculated in response to similar hypotheses and found to render them mathematically inconceivable, the true believers don’t care anyway. Neither math nor probabilities nor evidence can separate them from the faith they cling to.

  20. PaV, you do realize that, by equating “loss of function” with loss of information, you are calling half or more of all regulatory proteins and almost all regulatory zero- or negative (as in less than zero)- information entities. You may want to go there, but you won’t be doing your case any good.

    This is really simple – one more protein in the cmsT maize than in its parents. One MORE – that’s an increase by any reasonable estimation.

    One more thing – your focus on loss-of-function will take you in some directions that will make no biological sense. That is because the effects of T-urf13 are analogous in a developmental sense to the regulatory proteins that control programmed cell death during development. You may want to claim that, for example, digits are the results of losses of information, but you will have a hard time keeping biologists from smirking at the suggestion. (If that – if they are not aware of the reason you are making all this up, they will probably scratch their head and pat yours with either puzzlement or condescension.)

  21. You early suggested that Dr. Hunter should calculate the odds using a computer and expertise in biology and probability.

    I suggested nothing. I only asked if he was doing so.

    Why should anyone bother?

    You mean why anyone should undertake empirical study and communicate the results to support a claim they are expecting people to understand and adopt? I dunno, I’d think the answer to that question would be self evident.

    First, the premise is blatantly absurd. Should someone really get busy calculating and programming every time there’s another nonsensical theory that some complex component or feature miraculously invented itself.

    Well, if we were talking about Time Cube, I would agree. But, like it or not, there has been 150 years and untold thousands of papers published related to the study of evolution. If ID is going to become the reigning paradigm in the life sciences, it is going to have move beyond Monday morning armchair quarterbacking.

    I can understand if you don’t have the expertise to do such calculations. So, when I ask “you” to share the probability calculations, it isn’t a literal “you”, but rather a generic reference to any one who would make such a claim. Like Dr. Hunter, for example. He has a PhD in Life Sciences and is employed by a major university that is obviously supportive of his work. He is perfectly situated to do work through the probabilities. I hope that he is doing so and look forward to his response.

    Second, when the most optimistic odds possible are calculated in response to similar hypotheses and found to render them mathematically inconceivable, the true believers don’t care anyway.

    So, someone has actually calculated the probability of a specific feature to be formed through evolution? Cool. Can you point me to where this is? Or are you making another claim based on what you think is true rather than what you have evidence that is true?

  22. One more thing, PaV. You claimed:

    From the papers I looked at during that, let us say, discussion, the bottome line seems to be that T-urf13 results when URF-13 becomes degraded; that is, it involves a “loss of function”.

    This is wrong. Not only do the quotes you provide say no such thing (and to claim as much is to badly misrepresent the various authors), it is well established that the cms-associated biochemical characteristics require an intact and functional protein. Heck, the last two sentences of the quote you provide in #10 say as much.

  23. This is really simple – one more protein in the cmsT maize than in its parents. One MORE – that’s an increase by any reasonable estimation.

    And increase in what?

    Funny, Art here arguing for an increase in something that biologists, when they dare speak of it, do so only in a colloquial and informal way.

  24. hummus man:
    You mean why anyone should undertake empirical study and communicate the results to support a claim they are expecting people to understand and adopt?

    Way to shift the burden of proof. Exactly what such study supports the undirected evolution of complex new genes such as T-urf13? No, we’ll start from that assumption, and anyone who questions it must demonstrate that it’s false.

    I hope you don’t develop medicines. Assume it’s safe and treats the condition, and if really does nothing or makes people sicker, it’s someone else’s job to figure that out. And they’d better have their pencils sharpened.

    Why should anyone go to such lengths (and yes, they have) to challenge your faith-based assumptions? There’s no reason to take it seriously.

  25. hummus man,

    Evolutionists can’t even describe the methodology used to determine that “evolution” is blind and undirected.

    Not only that there aren’t any peer-reviewed papers that demonstyrate useful complex protein machinery can arise via mutational accumulation.

    And nothing that shows body plans can be changed.

  26. Take the phrase “Methinks it is like a weasel”.

    Then duplicate a word:

    “Methinks it is like like a weasel.”

    Do we have an increase of information? No. More characters but not more information.

    But hey we added ONE MORE WORD!

    Now mutate that duplicated word”

    “Methinks it is lite like a weasel.”

    Do we have more information now? Again no.

    And if we continue to mutate we could end up with:

    “Methinks it is not like a weasel.”

    The original information has been replaced by its opposite.

  27. Scott Andrews:

    Way to shift the burden of proof.

    It is generally accepted that the person making the claim bears the burden of proof to support it. Evolution is an extraordinary claim and has spurred 150 years of research that supposedly supports it. Dr. Hunter claims that evolution is probabilistically impossible, but has not provided any indication that he has done anything to support the claim. And it is your position that the person making a claim has no responsibility to support it?

    I hope you don’t develop medicines. Assume it’s safe and treats the condition, and if really does nothing or makes people sicker, it’s someone else’s job to figure that out. And they’d better have their pencils sharpened.

    That is a good synopsis of your (and presumably Dr. Hunter’s) position. Throw the claim out there that evolution is probabilistically impossible, but leave it to someone else to actually calculate the probabilities.

    Why should anyone go to such lengths (and yes, they have) to challenge your faith-based assumptions? There’s no reason to take it seriously.

    The Darwinists at least go to the effort of trying to support their claims. It may be Kabuki theater, but at least they are putting some effort into it. You are doing exactly nothing. There is a seriousness gap here, but it is not where you think it is.

  28. hummus man:

    It is generally accepted that the person making the claim bears the burden of proof to support it.

    Your position claims that humans “evolved” from non-humans via an accumulation of genetic accidents.

    Yet no one has ever supported that claim.

    As a matter of fact the ONLY claims you have supported support baraminology.

  29. Arthur Hunt:

    This is really simple – one more protein in the cmsT maize than in its parents. One MORE – that’s an increase by any reasonable estimation.

    From what I remember of the literature I looked at, a third of the URF13 protein is ‘lost’ in the production of T-urf13. Now I suppose that means that one of the introns that is usually connected to the other two introns in forming URF13 is either completely corrupted or completey eliminated. I suspect it is just simply eliminated. Now, unless you want to claim that DNA nucleotide sequences contain no information whatsoever, then this loss or corruption represents a loss of information. T-urf13 can no longer perform the function of URF13; this is because it has lost the proper ‘information’ it needs. This is quite clear, isn’t it?

    Not only do the quotes you provide say no such thing (and to claim as much is to badly misrepresent the various authors), it is well established that the cms-associated biochemical characteristics require an intact and functional protein. Heck, the last two sentences of the quote you provide in #10 say as much.

    I didn’t necessarily say that the quote I was providing said that. I said that “from the papers I read” while having our discussion, I remembered the degradation–which occurs, IIRC, in the mitochondria through all sorts of ‘recombinant’ events which has the effect of degrading once section of the URF13 protein.

    Now I’m sure URF13 is present and performs other functions, but it is the presence of T-urf13 that brings about cytoplasmic male sterility (cms).

    The very last sentence of the quote says that “no such molecule has been found.” So, it is saying that if the thesis is that a ‘gain’, and not a loss, of function is at play, this can’t be validated through the presence of a ‘biosynthetic’ molecule.

    As to loss-of-function in general, if you take a Maseratti and tear out the passenger seat, break out the rear window, and smash down the rear end, I’m sure you can now ‘store’ more material aboard as you drive along, but I’m rather sure everyone would now say that the Maseratti is a bit “degraded”. If you turned a Toyota corrolla into a Maseratti, now that’s something.

  30. Joseph, having observed discussions with you elsewhere, I am pessimistic that this will go anywhere. But, I have one question.

    As a matter of fact the ONLY claims you have supported support baraminology.

    How many original kinds were there and how long ago were those original kinds created/designed?

  31. hummuas man:

    How many original kinds were there and how long ago were those original kinds created/designed?

    That is what science is for- to help us ascertain those answers.

    If we knew all the answers we wouldn’t need science, would we?

    HOW can we answer those questions?

    By trying to figure out what it is EXACTLY that makes each organism (population/ type) what it is.

    And then try to figure out how much variation is permitted.

    But anyways what do YOU have?

    Do you have ANYTHING besides a refusal to accept the design inference that supports your position?

  32. hummus man:
    The Darwinists at least go to the effort of trying to support their claims.

    They’re supposed to score points for trying? Fine, A+ for determination, but I’ll start being impressed when they start succeeding. Until then, their dogged determination to confirm what they’ve already chosen to believe looks like ideology barely disguised as science.

  33. Joe responds to me:

    How many original kinds were there and how long ago were those original kinds created/designed?

    That is what science is for- to help us ascertain those answers.

    If we knew all the answers we wouldn’t need science, would we?

    Fair enough. All science is provisional, so it was an unfair question. Mea Culpa. Let me rephrase it. How many original kinds have been identified to date and what is the working hypothesis regarding how long ago those original kinds created/designed?

    But anyways what do YOU have?

    You mean besides an odd desire to see if you’ll actually answer my question? Not much that you would accept anyways. So, let’s just say I got nuthin and clear the decks so you can hold forth on the number and age of the known baramins.

  34. PaV @ #29:

    From what I remember of the literature I looked at, a third of the URF13 protein is ‘lost’ in the production of T-urf13.

    You remember quite incorrectly. There is no T-urf13 gene in any of the cmsT progenitors.

    Why are you making all this up? The story is as I explain here. There is nothing in the literature about URF13 degradation being required for the cmsT trait.

    Maybe you need to provide an explicit reference that leads you to make these claims.

    And I’m impressed (in a sort of way) that you think digits are regressive compared with webbing. Would you like to look at a longer list of biological characters that are controlled by degradation? Are you seriously going to argue that this mechanism is always one that subtracts from an organism?

    (I don’t suppose it needs to be pointed out that the Maseratti analogy only drives home the point that biology and engineering are two quite different, usually diametrically opposite, propositions. But I’ll thank PaV for making the point for me; the more voices that are showing this, the better.)

  35. But anyways what do YOU have?

    hummus man:

    You mean besides an odd desire to see if you’ll actually answer my question?

    IOW you don’t have anything but a desire to misunderstand and misrepresent ID all the while never supporting your position.

    Got it.

    I don’t generally deal with intellectual cowards like yourself, I just expose them for what they are.

    BTW my point is all you have evidence for is slight variations.

    And nothing that shows those slight variations can accumulate in such a way as to support your position.

  36. Joe:

    IOW you don’t have anything but a desire to misunderstand and misrepresent ID all the while never supporting your position.

    Got it.

    Yup, you figured me out.

    Now, about those baramins. How many have been identified and what is their hypothesized age?

  37. hummus man:

    Yup, you figured me out.

    It wasn’t hard- all evolutionists are basically the same.

    Only the sock (puppet) changes, depending on the forum.

    Now, about those baramins.

    Baramins rule!

    Go baramins!!!

    Who dat? Who dat? What dat goin’ to beat those baramins?

    How many have been identified and what is their hypothesized age?

    This is the latest I can find:

    The Current Status of Baraminology-

    If you send an email to the author he may be better suited to give you an update.

  38. But anyways doesn’t it seem just a little odd that when really pressed for evidence that supports their claims all evolutionists can do is point to slight variations that have no chance of doing what is being debated?

  39. This is the latest I can find:

    The Current Status of Baraminology-

    If you send an email to the author he may be better suited to give you an update.

    Yeah, I can see now why you can’t answer questions.

  40. hummus man:

    Yeah, I can see now why you can’t answer questions.

    Right, lack of resources required to address such a complicated issue.

    OTOH your position has all the resourses and still can’t put together a coherent argument.

    Go figure…

  41. Right, lack of resources required to address such a complicated issue.

    DNA Sequencer too expensive to add to your basement laboratory?

  42. Obviously brains too expensive to add to your inventory.

    Perhaps you should go buy a vowel…

  43. Perhaps you should go buy a vowel…

    I would love to get my hands on a nice æ, but the radical Alphabetists have suppressed the evidence of the superiority of Olde English.

  44. I would love to get my hands on a nice æ, but the radical Alphabetists have suppressed the evidence of the superiority of Olde English.

    It was evolution by natural selection…

  45. Arthur Hunt:

    Art, I suspect that cms has been studied because of its commercial applications. It has not been well-studied. It was studied mostly in the 90’s. Not much interest has been shown since. If you look at the following quotes, it is apparent that URF13 is problematic for plant cells—as well as insect, worm and E. coli cells. The final sentence below says: “This male sterility gene is T-maize anther-specific and its origin is a genetic enigma.” So, here we have a gene that produces a protein that causes cell death, basically, and whose origin is enigmatic—-and, of course, is non-nuclear and thus non-Mendelian.

    The Mendelian equivalent to all of this seems to me to be balanced polymorphisms, such as sickle-cell anemia. Now, when you compare a sickle cell to a normal cell, would you say that it is better or worse? Functionally we know the answer is that its “fitness” is lower. In the case of cms, it would seem that in nature this kind of deformation which T-urf13 causes is very likely lethal, though there might be some unknown advantage. Nevertheless, it is only because commercial companies can provide a seed that is heterotic and nonetheless does not need crossing that the issue of cms of any importance whatsoever. However, now we’re dealing with artificial selection, and not natural selection.

    But maybe you would like to provide more information—because there surely is not much out there, and it’s old, and, quite frankly, I’m not really interested in looking further. I suspect you work with commercial grain companies and hence your interest in T-urf13; but this places you in a very small circle of people.

    Quotes taken from: Hybrid Cultivar Development by Surinder S. Banga Springer-Verlag 1998

    An interesting feature of male sterile T-cytoplasm maize plants is that their mitochondrial genome produces a 13-kDa polypeptide (URF-13) which is unique to this cytoplasm and absent in other maize cytoplasms . . . Unlike the larger open reading frame, which hybridizes to transcripts from all maize cytoplasm, the smaller open reading frame hybridizes to the transcripts available only in the T-cytoplasm and not to those of other sterile or fertile maize cytoplasm. Thus the T-urf13 sequence (115 codons) is unique to the mt genome of male sterile T-cytoplasm plants and is composed of sequences sharing homoloyg to the 3’-flanking (88 codons) and the coding region (18 codons) of the 26S r RNA gene, together with nine codons of unknown origin. . . .

    In order to ascertain if the 13 kDa protein (designated URF13) encoded by the T-urf gene is involved in this specific sensitivity of T-mitochnodria to T-toxin, the T-urf13 gene was cloned and transferred to E. coli by Dewey et al. (1988). This gene expressed in E. coli cells and caused inhibition of whole cell respiration and growth, massive ion leakage, and spheroplast swelling. . . . Thus, the interaction of T-toxin and URF13 results in sensitivity by permeabilizing the membranes of the bacterial cells and T-mitochondria. . .

    These authors demonstrated that the expression of the universal code equivalent to the T-urf13 gene in the yeast nucleus mimics its effects in maize, viz. respiratory growth of yeast is inhibited, respiration deficient cytoplasmic mutants . . . accumulated and NADH oxidation of the isolated mitochondria is coupled. . . These observations provide direct evidence that URF13 is responsible for the susceptibility of T-mitonchondrial genomes to fungal toxin, and male sterility is due to anther mt dysfunction caused by the T-urf13 gene. . .

    . . . After adding T-toxin or methomyl to the in vitro cultured fall army worm cells, permeabilization of the plasma membrane occurs. Furthermore, the gene URF13 is toxic to these in vitro cultured insect cells even without T-toxin or methomyl addition. . . .

    .
    .
    .
    . . . Because mutations in or deletions of the T-urf13 gene are associated with both the loss of male sterility and disease susceptibility, URF13 appear to be directly responsible for both these traits in T-cytoplasm maize. . .

    This male sterility gene is T-maize anther-specific and its origin is a genetic enigma.

    Arthur also said:

    And I’m impressed (in a sort of way) that you think digits are regressive compared with webbing. Would you like to look at a longer list of biological characters that are controlled by degradation? Are you seriously going to argue that this mechanism is always one that subtracts from an organism?

    When I was seventeen, I ended up with a thyro-glossal duct cyst, which had to be operated on twice. The reason for this was that the cyst came about because the thyro-glossal duct did NOT degenerate in utero. So I’m all in favor of ‘nature’ degenerating things. But you are trying to place the same importance on the degeneration of the thyro-glossal duct as anyone would put on the formation of the thyroid, for which the thyro-glossal duct temporarily exists.

    I just love Darwinists. How does natural selection work? Through species becoming more fit. How do species become more fit? Through natural selection. How does life come about? Through natural selection. How does natural selection work? Through selective death. Thus, life through death. Or progress through degradation. Is there any objectivity out there in Darwinland anywhere?

  46. Re PaV @ 45:

    1. CMS is studied actively and with much earnest at the present. T-urf13 hasn’t been (very much) studied for years, mainly because its origins and modes of action have been worked out (your claims the contrary notwithstanding).

    2. CMS is a naturally-occurring characteristic in plants, and plays roles in the evolution of different sexual reproductive strategies (in the wild as well as in breeding programs). A useful google term – gynoecious.

    Now, I rather suspect that you will claim that two “genders” – hermaphrodites and females – is less than one gender, but this is but another way that antievolutionists fail math.

    3. Characteristics in living things that are controlled by degradation (a very tiny fraction of the complete list, but …): circadian rhythms, brains, the cell cycle, flowering, sexual reproduction, asexual reproduction, mitosis, meiosis, etc., etc., etc.

    “Progress through degradation” is a fact of life (in every sense of the phrase). That this fact confounds ID tenets is just another nail in the lid of ID’s coffin. That ID proponents choose to pretend that this process doesn’t exist and cannot possibly contribute anything adds more to the disconnect between ID and biological reality.

    PaV, I rather suspect that you don’t have a clue here about the interesting molecular mechanisms (including degradation) that work to build up complexity in living things. Digging in your heels and responding with nervous laughter and rank incredulity is no way to “win” a discussion, let alone learn something.

    That point notwithstanding, when it comes to the status and stature of ID, we’re really accomplishing a lot with this discussion.

  47. Arthur Hunt,

    PaV, I rather suspect that you don’t have a clue here about the interesting molecular mechanisms (including degradation) that work to build up complexity in living things. Digging in your heels and responding with nervous laughter and rank incredulity is no way to “win” a discussion, let alone learn something.

    Nor is this sort of speculation about how another commenter feels. Did you hear nervous laughter over the written words? Did you smell the incredulity to decide that it was rank? This is no way to comment here or you will not be commenting anymore. Yes, this is a warning.

    “Progress through degradation” is a fact of life (in every sense of the phrase).

    This is a very confused philosophical position. Degradation doesn’t progress unless you use the term “progress” to mean something like decomposition. But no one would say that decomposition is a progression of life, it is a digression. Degradation is a digression.

  48. Another Art Hunt strawman:

    “Progress through degradation” is a fact of life (in every sense of the phrase). That this fact confounds ID tenets is just another nail in the lid of ID’s coffin. That ID proponents choose to pretend that this process doesn’t exist and cannot possibly contribute anything adds more to the disconnect between ID and biological reality.

    Dr Spetner covered that in 1997, Art.

    IOW once again you display ignorance of your opponents and think that ignorance is meaningful discourse.

    Also BEFORE you can start degrading to get progress you FIRST have to build to that point.

  49. The status and stature of the theory of evolution:

    They cannot even provide a working/ testable hypothesis based on their proposed mechanisms of accumulating genetic accidents.

    Art must be real proud of that…

  50. Arthur:

    Something from nothing, life from death, and progress through degradation are not part of ID. Somehow I don’t think that detracts from ID in the least.

    To vainly attempt to get across to you, I point out to you that ID is concerned with the ‘build-up’ of information, not its degradation. Degradation is simply a class of processes that brings about important results biologically and elsehwere (microchips are ‘etched’, for example). But, as “Joseph” points out, we here at ID are interested in the progressive end of evolution. Microevolution is ceded by most, but macroevolution—which is progressive evolution—is what we refute.

    You’re bringing an aracane argument to UD and trying to use it as a sledgehammer. It won’t work. You say cms is still being studied . . . . . but, of course, since it has agricultural applications and ‘Big Ag’ is interested. But there is simply no interest in Turf13. No one is studying it. The most recent review article—which I quoted at your blog—recycles old information indicating that the ‘jury is still out’ on whether turf13 works by ‘addition of function’ or ‘loss of function’. More likely, it is through ‘loss of function’. That appears to be the current state of things, and no one seems interested in finding out more. If turf13 represented a definite ‘addition of function’, and we had some sense as to how that happened, then that would be of interest here. Since neither of the above happen to be the case, I think I’ve probably said my last about it.

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