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De Novo Genes: The Evolutionary Explanation

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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
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.PaV
December 1, 2009
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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...Joseph
November 27, 2009
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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.Joseph
November 27, 2009
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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. Clive Hayden
November 26, 2009
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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.Arthur Hunt
November 26, 2009
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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?PaV
November 26, 2009
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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...Joseph
November 26, 2009
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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.hummus man
November 26, 2009
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Obviously brains too expensive to add to your inventory. Perhaps you should go buy a vowel...Joseph
November 26, 2009
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Right, lack of resources required to address such a complicated issue. DNA Sequencer too expensive to add to your basement laboratory?hummus man
November 26, 2009
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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...Joseph
November 25, 2009
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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.hummus man
November 25, 2009
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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?Joseph
November 25, 2009
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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.Joseph
November 25, 2009
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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?hummus man
November 25, 2009
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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.Joseph
November 25, 2009
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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.)Arthur Hunt
November 25, 2009
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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.hummus man
November 25, 2009
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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.ScottAndrews
November 25, 2009
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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?Joseph
November 25, 2009
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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?hummus man
November 25, 2009
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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.PaV
November 25, 2009
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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.Joseph
November 25, 2009
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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.hummus man
November 25, 2009
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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.Joseph
November 25, 2009
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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.Joseph
November 25, 2009
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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.ScottAndrews
November 25, 2009
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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.Mung
November 24, 2009
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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.Arthur Hunt
November 24, 2009
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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?hummus man
November 24, 2009
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