De Novo Genes: The Evolutionary Explanation

_{Cornelius Hunter

November 23, 2009

Intelligent Design}

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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

Comments

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.)Arthur Hunt_{November 24, 2009
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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.ScottAndrews_{November 24, 2009
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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.Joseph_{November 24, 2009
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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.Joseph_{November 24, 2009
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tgpeeler, Thanks for the reference. I will add it to the list.Joseph_{November 24, 2009
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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.hummus man_{November 24, 2009
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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. fGfaded_Glory_{November 23, 2009
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Joseph, I can also recommend Dean Overton's book, A Case Against Accident and Self-Organization.tgpeeler_{November 23, 2009
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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.Joseph_{November 23, 2009
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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.Joseph_{November 23, 2009
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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.).PaV_{November 23, 2009
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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.ScottAndrews_{November 23, 2009
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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/10.1101/gr.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-URF13Dave Wisker_{November 23, 2009
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"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.jerry_{November 23, 2009
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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?osteonectin_{November 23, 2009
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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.Collin_{November 23, 2009
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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.jerry_{November 23, 2009
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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?hummus man_{November 23, 2009
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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).Collin_{November 23, 2009
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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?faded_Glory_{November 23, 2009
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