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Author | Topic: Darwin in the Genome | |||||||||||||||||||||||||||
derwood Member (Idle past 2126 days) Posts: 1457 Joined: |
Another 'unanswered letter'....
One day when I was a graduate student, I brought my advisor his mail from the department office. As we chatted, he leafed through the many letters and larger envelopes he received that day. One had some dinosaur stickers on it. It caught his attention. It was a letter from one "Kelly Segraves", who, if I am not mistaken, is or was at one time a well known creationism advocate. The letter contained several "questions" regarding my advisor's work and the usual 'challenges' for him to 'justify' his conclusions based on the unsupported assertions made by him (Segraves). Which is odd, since my advisor worked with Primates, and most of these assertions and questions dealt with dinosaurs. My advisor chuckled and tossed it into the garbage. I can only imagine that this Segraves, upon not getting a response for several weeks, declared that because there was no response, there must have been bo good answers to his questions and that therefore he (Segraves) must be right. Borger - an unanswered "letter" is more likely a sign that the recipient found its contents unworthy of reply, rather than the recipient being 'troubled' by the implications. Up your dose.
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Adminnemooseus Inactive Administrator |
quote: I, in the minnemooseus mode, have not taken part in this thread, or for that matter, much if any part, in any "Evolution" topic. As minnemooseus, I have previously started a "Suggestion" topic, which suggested that Peter Bourger and his ideas might be best served by (at least for now) confining them to one topic (such as William Scott has done with his flood ideas). I don't think that Peter Bourger's "scatter shot" presentation of his GUToB is doing a service to to either his ideas, or to the discussion being done in the various topics. I'm rather confident that the official forum guidelines can give me a weapon towards guiding Mr. Borger towards a more unified discourse on his theory, should push come to shove. Right now, I just wish to STRONGLY encourge Peter to take his theory to a single topic location, so that we can coherently discuss it's merits. There is a GUToB topic in the "Welcome, Visitors" forum. I don't know why it was started in that forum, but perhaps it best be moved to "Evolution". Maybe I should make this message it's own topic. We'll see. Adminnemooseus ------------------{mnmoose@lakenet.com}
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
Hi Page,
I am trying to understand genetic redundancies in the light of evolution as a random process (=random mutation plus selection). Redundant genes usually demonstrate only moderate sequence homology.For instance the alpha-actinin genes. The a-actinins comprise a group of actin-binding proteins encoded by a multigene family. In skeletal muscle, they are a major structural component of the Z-lines that anchor the actin-containing thin filaments and maintain the spatial relationship between myofilaments. In humans, two genes (ACTN2 and ACTN3) encode the closely related a-actinin-2 and a-actinin-3 skeletal muscle isoforms. ACTN2 is expressed in all skeletal muscle fibres, whereas expression of ACTN3 is limited to a subset of type 2 (fast) fibres. A careful screening of muscle biopsies with dystrophic (118 specimens), myopathic (74), neurogenic (20) and normal (55) features demonstrated that all specimens contained normal a-actinin-2 expression. Deficiency of a-actinin-3 was identified in 51 of the 267 cases (19%), and was due to a common non-sense mutation that introduced a premature stop codon. So, the proper a-actinin-3 protein cannot be synthesised. Surprisingly, the deficiency was not associated with any particular histopathological or clinical phenotype [North et al, Nature Genet.1999, 21:353]. What troubles me is that I cannot think of a molecular mechanism that gave rise to such genes. According to theory, duplication and divergence gave rise to the alpha-actinins. A close look at the redundant genes reveals that the differences are the result of single nucleotide mutations. Neutral evolution rate is about 10(exp)-9/nucleotide/year, and recent genome wide studies present evidence that purifying selection worked upon duplicated genes (Dr Wagner in Genome Biology). The ACTN2 and ACTN3 genes are approximately 3000 bp, and share 85% sequence homology. Moreover, the ACTN3 gene is highly conserved within mammals, suggesting ancient duplication and rapid diversion. I have a couple of questions regarding the evolutionary mechanisms involved in genetic redundancies. Since you are the PhD-ed evo biologist on the board they should be easy to address. I was hoping that you can find the time to address them: 1) Do these data mean that approximately 450 bp changes occurred on neutral positions? 2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? And 150 million years for 450 neutral mutations? 3) Do these data indicate that after each point-mutation there was (neutral) purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes? 3a) Is it independent from nearby genes? Independent from the rest of the genome? 3b) Does this type selection take place on the level of the organism? How? 4) Are recently duplicated genes present in the human genome? 5) Is evolution of the a-actinins driven by random mutation, or rather NRM? I hope you can help me out with my questions. I would be very grateful. Thanks in advance.(If you wish, we could discuss the src phosphatases later). Best wishes,Peter
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
Page says:
'Borger - an unanswered "letter" is more likely a sign that the recipient found its contents unworthy of reply, rather than the recipient being 'troubled' by the implications.' Borger says: 'If such were true, why do I respond to your letters?' Best wishes,Peter
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
Page and Paul,
Paul's quote:-------------------------------------------------------------------------------- If I remember correctly he didn't actually acknowledge that he WAS the asthma researcher. He certainly didn't volunteer the information, and I very much doubt that "our" "Peter Borger" (if that is his real name) has any real scientific qualifications. After all a medical researcher would probably have to know enough statistics to understand the importance of sample size, which this Peter Borger seems not to grasp at all. -------------------------------------------------------------------------------- PB: If I remember correctly (and I do), PaulK wasn't even registered to the board in those days.And a bout sample size. It has nothing to do with the example. Ever heard of random tests? Statistics too. Page: You may have a point. Way back, when Borger first started posting here, there was some discussion on this. I felt that he just happened to have that name, or perhaps co-opted it for discussion purposes, and ran with it. Schraf I think it was posted a list of citations from Pubmed. Borger has since written that "someone posted my CV" on EvC. He says "part of it". The problem is, not all of the citations were by the same P. Borger. So he sould well be an imposter.it would explain a lot. PB: From your little chat above, your 'psyches' become crystal clear. Thanks for providing clearance (although it was already obvious). It explains all. And, the problem is not whether the citations are from the same P. Borger or whether he is an imposter. The real problem is that evo's don't understand their own theory. That's the REAL problem and you don't wanna see it. [And I really don't understand you guys: if he's an imposter why waste your precious research time here? Why not follow Dawkins advice?] have a nice day,Peter
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PaulK Member Posts: 17907 Joined: Member Rating: 7.3 |
Firstly one can read the board without being registered as I did for some time.
Secondly your lack of understanding of the importance of sample ssize is based on the discussions of human mtDNA where you dismissed the importance of using a larger sample. Thirdly you are the one who does not understand evolutionary theory as indicated by your own refusal to explain the sense in which the theory requires mutations to be random, and thus support your claim that the "non-random" mutations contradict this. In the absence of any such explanation it is clear that your "refutation" relies on a point of evolutionary theory that you do not even understand well enough to discuss. Which demonstrates that you do not even understand your own argument. Your equation of purifying selection with some imaginary idea of "neutral selection" further underlines your lack of understanding.
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Percy Member Posts: 22931 From: New Hampshire Joined: Member Rating: 7.2 |
Hi Peter, welcome back!
There were a few issues that were raised before your brief absence that you haven't addressed. In Message 131 Scott says that he thinks your statement about alpha actinins ignores published literature, for which he provides a reference. I also addressed the actinin issue in Message 135. PaulK provides additional argument in Message 133. They all point out different ways in which your alpha actinin evidence doesn't support your premise. In Message 132 Scott pointed out the false logic you use to reach your conclusion about how novel genes originate. I also pointed out the same thing in Message 135. Concerning the unanswered letter, you mentioned it in Message 126 to support your actinin argument, and the point made in my Message 135 was that no conclusion can be reached from an unanswered letter. Scott was merely making the same point in Message 136. The bottom line is that you still haven't provided any rebuttal to the arguments pointing out the weaknesses of your actinin evidence. And in Message 137 Adminnemooseus has some requests concerning bringing some focus to discussion of your theory. --Percy
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Brad McFall Member (Idle past 5282 days) Posts: 3428 From: Ithaca,NY, USA Joined: |
Is not the *issue* whether one's "internal" 'map' that would hold the map idea TO the chromosome to be faulty because the linear nature of any and all gene expression is not the difference that one can "navigate" with a map but one can not navigate an organism??
I see this as a difference of issues dense in intelf that Piget held to be logical with the notion of space which is got from "reading" a map that IS NOT applicable to genomics + protenomics but need not follow Crick's criticism of Polyani either. The last clause of mine causes the problem for INTERPRETATION but the observation that a chromosome may be better if NEVER thought of as a map is preferable. The directum of mutations depends on the Neighboorhodd when not the Image as to what is "nonrandom" about it. We may be mislead genetically by thinking it interms of genomic mapping for any nautre of gene expression?
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derwood Member (Idle past 2126 days) Posts: 1457 Joined: |
quote: Isn't this the guy that conjures up imaginary particles ot 'explain' his alternative "theory"? Isn't this the guy that ignores evidence contrary to his claims and then insists that none has been presented? isn't this the guy that claims a book disproves NDT when the author of that very book expl;icitly said - in this thread - the opposite?Only to later say that the author is wrong and that yes, it does disprove NDT? Yeah, I guess it must be everyone else that doesn't understand evolution. It never is the megalomaniacal paranoid neurotic that imagines his troubles - it IS that everyone else is wrong and/or out to get him..
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derwood Member (Idle past 2126 days) Posts: 1457 Joined: |
Asking the same questions, making the same assertions, etc. over and over again will not change their irrelevance.
It would be nice if you could stick to topics at hand instead of trying to divert attention form your foibles every time you stick your head in your rectum. Tob Cap Oh - perhaps you should read and address the citation I presented on the a-actinin family. You can direct your list of questions to the authors of the paper. And be sure to tell them that you have disproved their work. Also, I have addressed the citation you provided on redundancies. Your questions seem to imply that, in fact, YOU didn't check it out, at least not in any depth. If you are going to produce citations that you claim prove your point, in the future it would be helpful to your position if they actually did. [This message has been edited by SLPx, 02-26-2003]
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
Hi Page,
I am still waiting. For the organisms that the abbreviations stand for and a phylo-tree. This is the third time I ask for it. I am not going to ask you another time (I have better things to do). So, if you wanna discuss your best evidence of commom descent in detail, this is your chance. best wishes,Peter
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
dear Paul,
PK: Firstly one can read the board without being registered as I did for some time. PB: Why? Dawkins' advice? PK: Secondly your lack of understanding of the importance of sample ssize is based on the discussions of human mtDNA where you dismissed the importance of using a larger sample. PB: My lack of understanding? What a poppycock. The only example of mtDNA sequences over time (0-62 Ky BP) we have at the moment can be regarded as a random sample. That this small is not in accord with evolutionism is tale telling and I predict that other ancient mtDNA sequences will demonstrate similar results as soon as they are published. I mentioned this before and you better listen to what I say. PK: Thirdly you are the one who does not understand evolutionary theory as indicated by your own refusal to explain the sense in which the theory requires mutations to be random, and thus support your claim that the "non-random" mutations contradict this. PB: No, since you are the evolutionist YOU are going to do that. Let's see what a man of the field makes of it. If you are defending your theory better explain it properly too. PK: In the absence of any such explanation it is clear that your "refutation" relies on a point of evolutionary theory that you do not even understand well enough to discuss. PB: I know all in and outs of this outdated theory and I know where and why it cannot hold in the light of contemporary findings. PK: Which demonstrates that you do not even understand your own argument. Your equation of purifying selection with some imaginary idea of "neutral selection" further underlines your lack of understanding. PB: The concept of 'weak purifying selection' has been introduced to "explain" genetic redundancies. For some families 'neutral purifying selection' has to be introduced to understand them in an evolutionary sense (as demonstrated, and denied by the evo-community, as expected). It is of course humbug, and evo's will not demonstrate such examples and that's why I do it. best wishes,Peter
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PaulK Member Posts: 17907 Joined: Member Rating: 7.3 |
I have no idea why you would think that I take advice from Dawkins on which internet fora I visit or how I approach them.
The section of mtDNA you considered cannot be considered a random sample - because it is not. And even a random sample has limitations which is why professional polling organsiations seek to obtain a balanced sample. And no, it is not the only relevant mtDNA that we have - as was mentioned in the thread. And of course you failed to even consider the significance of the fact that the sample offered by Dr. Page was of the same size. And I note that you still cannot explain the very point of evolutionary theory you claim to have refuted. What is even more amazing is that I have referred to it more than once and you still expect me to explain it again ! Clearly your claim to know "all the ins and outs" is false. And even if there are evolutionists who refer to "neutral purifying selection" - which I doubt - this still does not change the fact that the term neutral selection does not refer to purifying selection. In fact neutral selection is used to refer to the situation where neither purifying nor positive selection are operating. And as the referecnes I have discovered show, it is not the case that the knockout of the ACTN-3 gene is neutral even in humans (and it is certainly detrimental in other species).
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
Dear paul,
PK: I have no idea why you would think that I take advice from Dawkins on which internet fora I visit or how I approach them. PB: I can't understand why anybody would take advice from somebody who demonstrably does not know the most elementary stuff of the topic he discusses. PK: The section of mtDNA you considered cannot be considered a random sample - because it is not. PB: You owe the board an explanation. PK: And even a random sample has limitations which is why professional polling organsiations seek to obtain a balanced sample. And no, it is not the only relevant mtDNA that we have - as was mentioned in the thread. And of course you failed to even consider the significance of the fact that the sample offered by Dr. Page was of the same size. PB: Apparently you still don't get the example: it was on a 360 bp mtDNA region in ancient human mtDNAs (0-62 kY BP). Maybe you could provide the other references on ancient human mtDNA in several ancient human species. Maybe I should also mention that a good theory requires to be right in extreme conditions. For instance Einsteins' gravitational theory proven over and over through extraordinary predicted observation. The mtDNA could be such extraordinary case. It turns out to falsify evolutionary assertions. To me it is clear that evolutionism is a bad theory. PK: And I note that you still cannot explain the very point of evolutionary theory you claim to have refuted. What is even more amazing is that I have referred to it more than once and you still expect me to explain it again ! Clearly your claim to know "all the ins and outs" is false. PB: Great, I don't see your explanation. I offered you the opportunity but you simply let it go by.And I did not claim to know that all ins and outs to be false, I said that contemporary biology has severe implications for evolutionary theory. You make a strawman, and next attack the strawman. Not much of an argument. PK: And even if there are evolutionists who refer to "neutral purifying selection" - which I doubt - this still does not change the fact that the term neutral selection does not refer to purifying selection. PB: Why do you keep misrepresenting what I say? I said that very weak purifying selection has been introduced, and that I introduced neutral selection for certain genetic redundancies to explain them in an evolutionary sense. I wonder, how can one discuss with people who keep making up strawmen and keep misrepresenting. It is a debating tactic to wear the opposite party out, so the attack will be ceased, I guess. However the attack will not stop, the more you object to my claims the more I will show where your pet theory goes wrong. One thing that biology has taught us is that everything has to be in balance. PK: In fact neutral selection is used to refer to the situation where neither purifying nor positive selection are operating. PB: So, at last we know what neutral selection is. It is though a contradiction in terminis. Besides, from evolutionary theory it is to be expected that genetic redundancies mutate faster than essential genes. As recently demonstrated they do not (and mentioned several times in the discussions and backed up by scientific literature). PK: And as the references I have discovered show, it is not the case that the knockout of the ACTN-3 gene is neutral even in humans (and it is certainly detrimental in other species). PB: The data I have recently encountered on a symposium in Sydney demonstrate that the presence of a-actinin MAY have a positive effect on sprint performance, but is only significant in large groups. This shows that it is not necessary for sprint performance in a considerable amount of athletes: redundancy. And redundancies are going to be inactivated over time, as predicted by the GUToB. Best wishes,Peter
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peter borger Member (Idle past 7915 days) Posts: 965 From: australia Joined: |
Dear page,
Of interest:J Mol Evol 2003 Jan;56(1):1-10 The alpha-Actinin Gene Family: A Revised Classification. Dixson JD, Forstner MJ, Garcia DM. Southwest Texas State University, 78666, San Marcos, TX, USA, jamie.dixson@excite.com The sequencing of a genome is the first stage of its complete characterization. Subsequent work seeks to utilize available sequence data to gain a better understanding of the genes which are found within a genome. Gene families comprise large portions of the genomes of higher vertebrates, and the available genomic data allow for a reappraisal of gene family evolution. This reappraisal will clarify relatedness within and between gene families. One such family, the alpha-actinin gene family, is part of the spectrin superfamily. There are four known loci, which encode alpha-actinins 1, 2, 3, and 4. Of the eight domains in alpha-actinin, the actin-binding domain is the most highly conserved. Here we present evidence gained through phylogenetic analyses of the highly conserved actin-binding domain that alpha-actinin 2 was the first of the four alpha-actinins to arise by gene duplication, followed by the divergence of alpha-actinin 3 and then alpha-actinins 1 and 4. Resolution of the gene tree for this gene family has allowed us to reclassify several alpha-actinins which were previously given names inconsistent with the most widely accepted nomenclature for this gene family. This reclassification clarifies previous discrepancies in the public databases as well as in the literature, thus eliminating confusion caused by continued misclassification of members of the alpha-actinin gene family. In addition, the topology found for this gene family undermines the 2R hypothesis theory of two rounds of genome duplication early in vertebrate evolution. PB: The paper is on gene classification. And the explicit assumption that the one gene arose from the other. However, my comments posted to you yesterday questioned this scenario. It is my comments that I would like to have addressed, pubmed abstracts I can find for myself. Anyway, the final addition is interesting and in accord with Austin Hughes work: genomes can not be explained by chromosome duplications (e.g. Genome Res 2001, vol11, p771-780; J Mol Evol, vol48, p565-576). So, the only remaining possibility for genome expansion is duplication of preexisting genes and other DNA elements. This scenario is based upon assertions that duplication and divergence of the duplicates yield new genes. If genes are around that can not be explained accordingly (and they are), I see a little evolutionary paradox. [Also, preexisting sound a lot like........yep, GUToB] Page wonders: Who to believe? PB: That's a very good question. Although I do not object to the data, the evolutionary interpretation is questionable (at the least). Have a good one,Petey
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