Sternberg Plasters Matheson

_{Salvador Cordova

June 13, 2010

Biology, Darwinism, Science}

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“I think this will come to be a classic story of orthodoxy derailing objective analysis of the facts, in this case for a quarter of a century…The failure to recognize the full implications of this-particularly the possibility that the intervening noncoding sequences may be transmitting parallel information in the form of RNA molecules-may well go down as one of the biggest mistakes in the history of molecular biology.”

—John Mattick, Molecular biologist, University of Queensland, quoted in Scientific American

Steve Matheson, a teacher and Darwinist promoter at a religious school, repeats the biggest mistake in molecular biology. In contrast, Richard Sternberg, an evolutionary biologist at the Biologic Institute, defends objective analysis of the facts. See Sternberg’s defense of the facts against Matheson’s Darwinist ideology in the essay: Mathesons Intron Fairytale.

Comments

Phaedros, Not that I'm aware of except maybe for Dr. Hunter's blog. I posted some of my comments on Larry Moran's blog, this is how he responded to me:
Unfortunately for you, the human genome wasn't designed by an engineer, unless it was the same one who works for BP.
My response: so it's perefectly fine for Darwinists to apply their supposed design standards in evaluating systems (i.e. they label thinks junk at their own whim), but when I cite common engineering practice, somehow that's not a valid benchmark? There you have it from one of the trio. As far as PT goes, Art is one of the authors there. He would be the most able to respond, but as I said, I think he is mistaken. He's attacking arguments that Sternberg and Wells aren't making, imho. I will leave it to Art however to have his say regarding the objections several of us have put forward at UD.scordova_{June 15, 2010
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By the way, is everyone off debating on a different blog?Phaedros_{June 15, 2010
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Sometimes it seems incredibly difficult to reconcile or even attempt to synthesize these two outlooks on the evidence. It's like you have two extreme opposites, one where the glass is half full and one where the glass is half empty and there's no intermixing between the two.Phaedros_{June 15, 2010
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off topic Phaedros: the retina was addressed here recently by David Tyler: The contribution of glial cells to human vision acuity http://www.arn.org/blogs/index.php/literature/2010/05/10/the_contribution_of_glial_cells_to_human and here: The vertebrate eye does not have a compromised design http://www.arn.org/blogs/index.php/literature/2007/05/08/the_vertebrate_eye_does_not_have_a_compr and here: https://uncommondescent.com/intelligent-design/the-contribution-of-glial-cells-to-human-vision-acuity/ From looking over the PT article it is obviously "damage control" for a very embarrassing development.bornagain77_{June 15, 2010
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One observation and one question: Observation: It seems that Art Hunt and veilsofmaya come here to contest Sternberg and all they really have are rhetorical devices. (I am especially disappointed, but not entirely surprised, that gpuccio has discovered that the paper Art Hunt cites deals with almost esoteric cell lines---this is almost a kind of duplicity) Question (for both Art and veils): Tell me, which is more highly converved, the coding, or the non-coding, portions of DNA? (Would you like to talk about this?)PaV_{June 15, 2010
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off-topic, but has anyone done a substantial response to this at PT http://pandasthumb.org/archives/2010/06/more-creationis.html#morePhaedros_{June 15, 2010
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It actually is good design practice to make generic capabilities that are not too customized. This allows easy maintenance and manufacture.
Nothing like unrelated functions linked together, like hair color and texture, and tameness. Makes code maintenance a snap. When I worked as a programmer, I was required to make my code as cryptic and entangled as possible. I'd have been fired if I wrote something that the guy following me could understand and maintain without fear of breaking several unrelated functions.Petrushka_{June 15, 2010
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scordova, If you approve of Mattick's speculations, do you also agree with his assumptions of life beginning 4.2 billion years ago, common descent, and the Cambrian explosion as a natural event? Not that I agree that there is a positional cell type, but if positional data needed to be encoded in RNA, you could code for 10^12 positions in 20 nucleotides. 20. And the rest would still be junk. An interesting test of Mattick's ideas would be to see if there is any correlation between trancript complexity and weight. According to him, fat people need more complex RNA - so many more positions!Nakashima_{June 15, 2010
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Dr Hunt, Yes, I agree with you. It seems that Dr Sternberg thinks that each of the 7.6 introns per gene is involved in alternative splicing, rather than at least one out of the 7.6 introns, which is all that is implied by data. If each of the 7.6 introns was involved, then each gene would code for over 250 different proteins.Nakashima_{June 15, 2010
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gpuccio: So, for further clarity, I would like to formulate again the main question I formulated in my #47 to Arthur Humt about his interpretation of the Sultan paper, and which, I believe, has been restated in a slightly different way by scordova: Even if it were true that only 6% of the introns (indeed, of the reads) were involved in AS in the Sultan study, that is in two specific human cell lines, why should that mean that the other introns, all or most or many or some of them, are not involved in AS events in other human cell types and cell states?
EXACTLY! And the number of AS events which Sternberg discusses does not refer to the number of physical transcripts that emerge from the AS events but rather the number of varieties of transcripts. That is why I made the following distinction:
A charitable reading is 90% of the KINDS of transcripts existing emerged from alternative splicing. How can this be? a manufacturing analogy is inorder. Say we have 1000 cars, 900 of them are identical, but 100 of them are unique, and the unique cars emerged out of Alternative Manufacturing (Splicing if you will). Thus we have 101 different kinds of cars, and 100/101 = 99% emerged via Alternative Splicing. Thus even though 90% of the physical cars did not go through alternative splicing, 99% of the kinds of cars went through alternative splicing (so to speak).
And thus this invalidates the line of argumentation that focuses on a single cell type. The issue must make an estimate that includes the approximately 1,000,000,000,000 cell "types". Wells performed the method of estimation. We can clearly see Wells was not referring to sheer number of physical transcripts generated, but the number of different kinds of transcripts. Here is a rough calculation. Wells points out:
scientists reported that the majority of human genes generate almost eight different messenger RNAs.
Worst case 50% of genes have 8 different mRNA's. That means on worst case, on average each gene has 4 different mRNA, which implies, worst case 3 out of 4 alternative splices, or 75%. You can't just take one cell type and say, look, that gene had no alternative splices! That like picking a day a spare tire is not used and then saying, "see spare tires serve no purpose since on that day it wasn't used" or "the lexmark printer driver on Windows 7 serves no purpose because we saw Windows 7 users that didn't use that printer driver". I claim that Art is mis-using Sultan's paper in a similar way to make his point. I appreciate his participation here, but I think his line of reasoning is flawed. Finally, I should mention, it is perfectly reasonable that a cell has many unused or underutilized features. It doesn't make the features functionless any more than the unused features of Windows 7 among various Windows 7 users. It actually is good design practice to make generic capabilities that are not too customized. This allows easy maintenance and manufacture. The trade-off is that you have a lot of unused duplication. But we see from modern experience with operating systems, large amounts of unused function is the norm. We have little reason to say features of cell architecture won't have the same design features! In fact it is more consistent with the modern practice of complex systems engineering, particularly information intensive systems. Software engineers in particular will appreciate this fine point that seems to elude Darwinist biologists.scordova_{June 15, 2010
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That should be 20% in second to last paragraph, not 2%. Sorry about that, and any other typos that sneaked through. I'm especially having problems with my space bar, and it makes for rather interesting "words".Arthur Hunt_{June 15, 2010
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Sal, no matter how you try, you cannot twist Sternberg's and Wells' words to mean anything other than that they believe all introns (at least all introns in genes subject to alternative splicing) are themselves alternatively spliced. Heck, the unspoken consensus here seems to be in agreement with this. That is why there is so much effort to argue that, in fact, all introns do undergo alternative splicing. The suggestion that perhaps different sets of introns are subject to differential splicing in different cells or tissues is a good one. But there is nary an iota of evidence to suggest that the scale of such events even comes close to rescuing Sternberg and Wells from their gaffe. Some studies suggest a very modest scope of such events. IIRC (the paper is on another computer), the much-lauded "splicing code" paper used for confirmation studies an exhaustive set of some 11,000 or so alternatively-spliced exons (the much better unit to be talking about, reflecting yet another blunder on the parts of Sternberg and Wells, but that's another story altogether) that came from an analysis of many, many more than two cell types. OTOH, I am aware of no data - not a single study - that would support the suggestion that each and every intron may be subject to functionally-significant alternative splicing in at least one cell type. (Remember, were talking about a claim that there are more than 150,000 AS introns.) So, while the suggestion is fanciful and may be true to a rather limited extent, it hasn't the support of data to rescue Sternberg and Wells. There's one more bit of irony I haven't yet mentioned. The bigger picture here is the need by IDists to find function for the 1 billion + bp of intron-encoding DNA. Recalling again the "splicing code" paper (as well as one of the links I give), all of the intronic cis-elements involved in AS take up all of 600 nts (or less) of your generic AS intron. If each and every intron has 600 nts of such cis elements, that adds up to less than 2% of all intronic sequence. In other words, none of these considerations even makes a dent in the "junk DNA" problem. (I can see some confusion about the Sultan paper regarding what the authors mean by reads and sites. If this posting finds the light of day before Wed, I may add another one to explain things better,so readers are less confused by things.)Arthur Hunt_{June 15, 2010
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So, for further clarity, I would like to formulate again the main question I formulated in my #47 to Arthur Humt about his interpretation of the Sultan paper, and which, I believe, has been restated in a slightly different way by scordova: Even if it were true that only 6% of the introns (indeed, of the reads) were involved in AS in the Sultan study, that is in two specific human cell lines, why should that mean that the other introns, all or most or many or some of them, are not involved in AS events in other human cell types and cell states? Different cell types are defined by different transcriptomes. That means different genes involved, and very likely different AS events. It's perfectly reasonable to assume that, if 6% of introns are involved in AS in just two cell types, a greater number, probably a much greater number, will be involved in all possible AS events in the total set of human cell types.gpuccio_{June 15, 2010
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There is also a possible Equivocation in the way Art is arguing against Sternbergs claim:
At least ninety percent of gene transcripts undergo alternative splicing, and there are at least 190,000 introns in the human genome.
A charitable reading is 90% of the KINDS of transcripts existing emerged from alternative splicing. How can this be? a manufacturing analogy is inorder. Say we have 1000 cars, 900 of them are identical, but 100 of them are unique, and the unique cars emerged out of Alternative Manufacturing (Splicing if you will). Thus we have 101 different kinds of cars, and 100/101 = 99% emerged via Alternative Splicing. Thus even though 90% of the physical cars did not go through alternative splicing, 99% of the kinds of cars went through alternative splicing (so to speak). Hopefully the clarifies further the mis-use by Art of Sultan's paper. :-)scordova_{June 15, 2010
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The reason I mentioned spare tires and operating systems is that Art is referencing the behavior of a single cell type to make his case. There are, according to Mattick, 10^12 or 1,000,000,000,000 positionally differentiated cell types. I'd say even if Art makes a case for one cell type, (and I'm still disputing he got the account correct), he is making an awfully hasty generalization given we have, according to mattick 1,000,000,000,000 positionally differentiated cell types. :-) It would illegitimate to say that because you found a computer user that only uses 5% of Windows 7, therefore 95% of Windows 7 is non-functional! I claim Art's citation of from Sultan's paper is equally flawed. He is more than welcome to contest my characterization of what he said. Thanks in advance to Art for his response.scordova_{June 15, 2010
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Spare Tires and Operating Systems: I should point out there are legitimate and illigitimate ways of characterizing functions. It would be illegitimate to cherry pick all the days where spare tires on cars are not used. It would be illegitimate to say, "the spare tire wasn't used on July 19, 2001, therefore the spare tire serves no function". In similar fashion, it would be illigitimate to say certain features of an operating system (like Windows 7) aren't functional merely because we find computer users who don't use all the features of the operating system! We certainly might find introns in some cells that are not used, but it would be deeply improper to generalize the behavior of introns in one cell type to all cell types. In fact Mattick argues introns are used differently in each cell type. If indeed the cell uses operating systems like modern computers, and if cells have backup systems like spare tires, we would actually expect cells to have functional capabilities that are not always utilized. The lack of utilization 100% of the time is not evidence against function anymore than the lack of use of a spare tire or unused feature of an operating system is evidence against its function.scordova_{June 15, 2010
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V,
However, Mathasion clearly provided context when he use the phrase known to have “important functional roles.” Note the qualifiers “know to have” and “important functional roles”.
NOT KNOWING IF AN INTRON HAS FUNCTION DOESN'T MEAN THE INTRON HAS NO FUNCTION! GET A CLUE!scordova_{June 15, 2010
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@scordova (#42) It seems you analyzing Matheson's quote without using any context at all. If that's the case then, yes, it's impossible to say that anything couldn't have some vague function in some form or another at some point in time or some scenario. However, Mathasion clearly provided context when he use the phrase known to have “important functional roles.” Note the qualifiers "know to have" and "important functional roles". Removing these objections, it seems the real issue is that your merely offended by the idea for reasons that are theological in nature.veilsofmaya_{June 15, 2010
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ART asks: Are we all in agreement with Sternberg and Wells when they claim that every intron in every human gene whose RNAs are subject to alternative splicing are themselves alternatively spliced?
They did not make that claim, that is your mischaracterization. Also you have to make a distinction between the specific gene behavior in a specific cell type versus the collective behavior of the gene in all cell types where the gene exists. I'm afraid your EQUIVOCATING the behavior alternative splicing in one specific cell type when Wells is cleary discussing the collective involvement of introns in all cell types in the manner Mattick discusses them. By the way, Wells also references Sultan's papers.scordova_{June 15, 2010
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Sal, lightly skimming for articles on Introns, I found this: Introns -- Nonsense DNA -- Excerpt: And surprisingly, the vast majority of intron DNA sequences the scientists examined were of unknown origin.,,, Almost all of the introns the IU Bloomington biologists located possessed a sequence of indeterminate origin. Only one of the 24 identified sequences bore a resemblance to a specific DNA sequences associated either with the Daphnia genome or its parasites. The other 23 introns had sequences that appear to have been improvised by the machinery responsible for DNA synthesis. "Our molecular analyses have enabled us to reject a number of hypotheses for the mechanism of intron origins, while clearly indicating an entirely unexpected pathway -- emergence as accidents arising during the repair of double-strand breaks," Lynch said. http://www.sciencedaily.com/releases/2009/12/091210111148.htm You Know Sal, I think I am really beginning to love these intron sequences 8)bornagain77_{June 15, 2010
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Let me use a more everday example to clarify what I think Art's misreading is. The mistake is like saying:
6% of cars have GPS built in, therefore only 6% of cars with built-in GPS have a with built-in GPS have a GPS signal processor in their GPS system
the correct characterization is
6% of cars have GPS built in, but 100% of cars with built-in GPS have a GPS signal processor in their GPS system
Of course, in the case of introns we don't know for sure if 100% of all Alternative Splice events involve introns, but I'm claiming you can't make the inference that only 6% of all Alternatively Spliced events involve introns from Sultan's paper. I'm inviting Art to clarify, and I thank him for participating in this scientific exploration. Salscordova_{June 15, 2010
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For the reader, I'm claiming Art is making an incorret, non-sequitur inference from the literature he is citing (Sultan's paper). You can't claim that introns are only limited to be involved in only 6% of alternative splice events. The 6% figure only references the number of reads that are alternative splice events, it says nothing of proportion of Alternative splice events that involve introns. I consider this a technical mistake. We have in this particular case: 6% of reads are Alternatively Spliced Now take all those Alternative Spice events, what proportion of them involve introns? It is possible 100% could involve introns. You certainly can say since 6% of the READS are alternatively splice that therefore 6% of alternative spices involve introns. Such a conclusion does not logically follow from the premise, but constitutes a mis-reading of the literature. Art is welcome to defend his claim and correct mine (if I'm wrong). Thanks in advance Art.scordova_{June 15, 2010
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Art, You can't argue that a particular gene in an already differentiated cell implies the gene is limited to only 6% alternative splicing! You have to look at every cell that contains that gene!!!!! See Mattick's tally of the number of differentiated cells. You're basing your claims on 1 cell, whereas we might have to examine 10^12 positionally different cell types to make an exhaustive search. But based on diffentiation alone, it would seem that the facts accord better with Sternberg and Wells. I welcome hearing from you. Thanks for visiting. Salscordova_{June 15, 2010
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We observed 95% of the splicing events expected in this data set, given the current sequencing depth (Table 1) (16). We identified 4096 previously unknown splice junctions in 3106 genes, mostly called by single reads and unique to one cell type (Table 1). Many of these junctions were associated with actively transcribed genes exhibiting more exons than average, pointing to rare splicing events. Approximately 6% of all splice-junction reads identified AS events (6416 junctions in 3916 genes HEK and 5195 junctions in 3262 genes in B cells) (table S9).
Art, How can you say introns are involved in only 6% of the Alternative splice events. This paper says only 6% of the READS are alternative splice events, it says nothing of the amount of introns involved in those 6% of the reads that are AS events. Please clarify for our readers.scordova_{June 15, 2010
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(30) veilsofmaya:
@uoflcard You wrote:
i.e., argument from ignorance. </blockquote:But then wrote:
I’m still waiting for the evidence or model that makes it remotely reasonable to expect law and chance, devoid of intelligence, to create functional, complex, specified information, at least within the probabilistic resources of the history of the known Universe.
Should I assume you’re just as open to the idea that the possible “functions” of non-coding DNA could resolve many if not all of the supposedly insurmountable problems you’ve just mentioned?
Not exactly sure what you're implying here. First of all, I'm open to any idea. But the idea that non-coding DNA is possibly the source of the rest of the information in the genome just moves the goal posts. Where did THAT information come from? If it really is an amazingly complex algorithm capable of sculpting life, and it operates purely by law and chance (i.e. naturally), then it must contain more information than it creates. So where did that fCSI come from? Arguing that law and chance probably did not create the information of life is not an argument from ignorance (if that is what you were trying to somehow imply) anymore than arguing that the "flying spaghetti monster" doesn't exist is an argument from ignorance. We are not omnipotent, therefore we will always be ignorant, to some extent. So we choose which currently available explanation explains our observations most accurately. Right now there is nothing beyond extreme faith, or even the need for naturalism to be true, to believe that law and chance made all of the complex funcitons of life, including human consciousness. But we have another possible explanation for fCSI, one we observe and experience on a daily basis: Intelligence. This is vastly different than someone denying the possible funciton of an string of non-coding DNA. We are discovering new function of non-coding DNA on a weekly basis, it seems. It therefore seems naive (indeed, a true argument from ignorance) to deny function to any genetic string that has not been extensively studied.uoflcard_{June 15, 2010
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Jerry, Seeing as the most glaring mistakes in molecular biology have been made by people UNDERESTIMATING the complexity of the cell, I feel rather comfortable presupposing function for the "junk", and I don't mind "going to the wall", as you put it, at all, for I have a strong feeling it will be the neo-Darwinists going to the wall for their beliefs, and indeed being buried by that wall when the wall comes crashing down on them. Shoot I am so bold as to predict any completely non-functional part of the genome that may be found will be the result of degradation, and certainly not the result of evolutionary processes just spinning through gazillions of sequences in DNA code trying to find a that elusive functional sequence: Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 Evolution Vs. Functional Proteins - Where Did The Information Come From? - Doug Axe - Stephen Meyer - video http://www.metacafe.com/watch/4018222bornagain77_{June 15, 2010
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Not to put a fly in the ointment but the ID position in no way rest on the percentage of the non coding DNA that has function. It is certainly greater than zero and probably much less than 100%. The higher this percentage the stronger the ID case is but even if it is relatively low it does not make a dent in the ID argument. So argue all you want and make it interesting but everyone should keep in the back of their mind that the actual percentage may not affect the strength of the anti ID argument. If the percentage is fairly high then it is a very strong ID case and definitely weakens the anti ID position. If it is relatively low then it no way undermines the ID case nor weakens its position. ID can just not claim this particular point. What we have here is a desperate attempt to make sure the percentage is not high because that would be a devastating blow to the anti ID people. It may not be all that high and it will probably be years before we find out the truth. This is just a caution to the pro ID people. Do not go to the wall on this. The percentage could be fairly low and the complexity so overwhelming in the actual coding and regulatory parts that it boggles the mind that it could happen by chance. The remaining non functional DNA may be there as a result of an extremely functional process that is very complicated but well designed and which leaves excess DNA as a result.jerry_{June 15, 2010
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I got an novel idea Maya, Matheson, Hunt. Instead of dogmatically presupposing we are just a bunch of cobbled together junk, as only the most refined evolutionary thinkers are allowed to think, why don't we allow for the completely absurd notion that we could just possibly be ,,,, Fearfully and Wonderfully Made - Glimpses At Development In The Womb - video http://www.metacafe.com/watch/4249713 You are so beautiful - Joe Cocker http://www.youtube.com/watch?v=wlDmslyGmGIbornagain77_{June 15, 2010
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Correction: The citation above stops at "I don’t agree with you." The rest is mine.gpuccio_{June 15, 2010
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Arthur Hunt (#13): I have read the paper you quoted. It is very interesting, and rich of information. While I will certainly take some time to analyze it in detail, I would like to offer you a very simple methodological reflection, not about the paper itself, which I find intriguing and convincing, but about the inferences which you and others seem to derive from it. So, my point is very simple. The paper, even with many technical points which should be discussed, is trying to give a snapshot of the transcriptomes and, in some measure, of the AS events. But where? In two human cell lines, HEK 293T, which is a specific cell line originally derived from human embryonic kidney cells grown in tissue culture, and Ramos B cells, a human Burkitt's lymphoma cell line. So my question is: why are you inferring that the number of AS events observed in tghese two cell lines, even if we accept it as accurate, should in any way represent the total number of AS functional events in all human cell types and cell states? The point with transcriptomes is obviously that they are specific to a cell type, and even to a cell state. The observed transcriptomes are significantly different between the two cell lines used in the above research, which are not even normal human cells. So, we can certainly presume that other cell types (and cell states) will have different transcriptomes (and different AS events). So, if the general question is how many introns actively take part in AS events in the whole set of human cells, of every type and in every state, you cannot certainly infer the answer form a single study which takes into consideration only two specific transcriptomes, of two cultured human cell lines, one of which hembryonal and the other one neoplastic. So, I stick to my statement that the available evidence is perfectly compatible with an important role of introns in AS (I will not quantify how many are implied, simply because we have no way to know for certain, at present). And that is only part of the picture, because AS is only one of the possible functions of introns. As you yourself say:
As far as the functional vs. non-functional business, there is one key fact that IDists ignore in all of this. I refer, of course, to the fact that intronic RNA is made and then thrown away. We don’t call it “junk” because we don’t know if it does anything, we call it so because it is discarded. (OK, OK, so maybe we should be calling it “garbage DNA” instead of “junk DNA”.) As I learned on the 14th of May, and in many, many past discussions, the “garbage disposal” may be a central feature of the cell, required for all manner of molecular, physiological,and organismal function, but it is not on the IDists’ radar screen. I don't agree with you. Why do you think that IDists are not aware that intronic RNA is made and then discarded? First of all, practically everything in the cell is "made and discarded". Cells are typically "far from equilibrium" systems. Some structures are more stable, others more transient. But that's no reason to infer that the transient ones are less functional. On the contrary, they could be transient exactly because that is connected to their function. IOW, while mRNA has to migrate into the cytoplasm and direct protein synthesis before it can be discarded, intranuclear RNA, which includes intron RNA, is probably implied in quick and subtle regulatory functions, its time of survival can be critically important to those regulation networks. There is indeed a lot of current research about the regulatory role of nuclear RNA, but I am sure that you know that better than I do. Finally, about terms like "junk", or "garbage", and so on, you should know that the concept of "junk" has been used for years by darwinists to imply that 96% of the human genome was non functional and represented an accumulation of evolutionary errors. That has been considered by many as an important argument in favour of the darwinian model of evolution. Indeed, terms like "junk" or "garbage" are simply not justified, and never were. The only appropriate term would be "non protein coding DNA".
gpuccio_{June 15, 2010
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