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Author | Topic: molecular genetic proof against random mutation (1) | |||||||||||||||||||||||
peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
Dear mammuthus,
If an utterly hypothetical gene duplication --that has been proposed to explain the incongruence of gene trees and species trees-- is not to be found in the genome than something is wrong with the method. It is proof against common descent beyond any doubt, the rooting of gene trees cannot overcome it. The theory falls. That's it. Better get used to it. best wishes,Peter
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peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
Dear Mammuthus,
You say:"Ever going to present your hypothesis with the supporting data, how the theory is falsafiable, yada yada yada?" I say:Good to have you back. How was the holiday? Convention? In your absence I presented some sort of hypothesis. It says that all organsims have a multipurpose genome and that adaptations to environment can be induced either randomly, or by non-random protein/RNA mediated mechanism. It holds that there should be a lot of redundant genes in the genome of any organism. That is exacly what we observe. In contrast, the hype of evolutinism doesn't have an explanation for redundant genes. So, that in support of my hypothesis. Furthermore, by now I presented 4 examples that cannot be explained by random mutation, but rather involves non-random mechanisms. These examples are the 1G5 gene, the primate ZFY region, the redundant alpha actinin genes, and today I mailed to SLPx that the DNA shuffling in ticks and lizards is exacly identical. These examples all point in the direction of non-random evolution. The overturn of an established paradigm takes time, I know. best wishes,Peter
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peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
Dear SLPx,
You wrote in a previous mail I didn't see yet: "-------------------------------------------------------------------------------- quote:-------------------------------------------------------------------------------- Originally posted by peter borger: I say: "Read something on neutral evolution (NT). You will find out that according to NT genetic change is expected on third positions in AA codons (due to redundancy in the genetic code). They are not present for the major part of protein coding genes. I think that's a bit peculiar in the light that it took these organsims millions of years to evolve." best wishesPeter -------------------------------------------------------------------------------- Hi Peter, I was hoping that you could point out where in Kimura's works he explains that genetic change is expected on third positions in AA codons. I think what the creationist is doing is engaging in a classic cart-before-the-horse misrepresentation here. But, please, Peter, prove me wrong. I possess a collection of Kimura's works, and I am fairly certain that I will have the paper(s) you cite." I say:It is known that the redundancy in the genetic code leads to neutral positions on the third positions of codons. For instance, the aminoacid leucine can be coded by 6 different codons including CUU, CUC, CUA, CUG. A look at these 4 codons reveals that the third letter of the code is unimportant for determining the aminoacid. This is known as "wobble in the anticodon". The same accounts for the aminoacids valine, serine, proline, threonine, alanine, arginine, and glycine. So, these positions are not under selective constraint (neutral positions) and are expected to behave accordingly. I don't know whether Kimura also had these positions in mind, but I do. best wishes,Peter
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Mammuthus Member (Idle past 6475 days) Posts: 3085 From: Munich, Germany Joined: |
Hi Peter
[QUOTE]Originally posted by peter borger:
[B]Dear Mammuthus, You say:"Ever going to present your hypothesis with the supporting data, how the theory is falsafiable, yada yada yada?" I say:Good to have you back. How was the holiday? Convention? *************************************+ Thanks. Holiday actually. Went to Spain to tilt at windmills In your absence I presented some sort of hypothesis. It says that all organsims have a multipurpose genome and that adaptations to environment can be induced either randomly, or by non-random protein/RNA mediated mechanism. Problem 1: this is the same old issue of your using an inappropriate definition of random mutation. For example, if a portion of a gene is wrapped around a histone in such a way that it is more or less likely to suffer demethylation it will radically change the probability that you get C to T transitions. However, the C to T transition is still random. Problem 2: Define protein/RNA mediated mechanism of mutation generation. If you mean the lack of proof reading functions of reverse transcriptase for example the higher rate of mutation generated is fully expected and non-random. It holds that there should be a lot of redundant genes in the genome of any organism. Big problem 3: How do random or non random mutation in any way account for redundant genes? There is no connection between the first and second part of your hypothesis. Redundant genes have been known to evolutionary biologists for decades and have presented no problems for the theory. I can think of lots of ways off the top of my head for how do generate duplications and redundancy. And to use your own oft fallacious logic, until you prove each gene is really redundant and not in some way involved in another slightly different funcition your hypothesis is dead That is exacly what we observe. In contrast, the hype of evolutinism doesn't have an explanation for redundant genes. Problem 4: or 3b if you will. This statement is false. So, that in support of my hypothesis. Problem 5: this sentence makes no sense. Furthermore, by now I presented 4 examples that cannot be explained by random mutation, but rather involves non-random mechanisms. These examples are the 1G5 gene, the primate ZFY region, the redundant alpha actinin genes, and today I mailed to SLPx that the DNA shuffling in ticks and lizards is exacly identical. These examples all point in the direction of non-random evolution. Problem 5: On multiple occassions it had been pointed out to you that your definition of non-random is wrong and is in conflict with what statisticians and evolutionary biologists use. That you choose to ignore this fact does nothing to further your cause or support your beliefs. The overturn of an established paradigm takes time, I know. It takes even longer when there is no compelling hypothesis or data with even a billionth of the support evolution has best wishes,M
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Mammuthus Member (Idle past 6475 days) Posts: 3085 From: Munich, Germany Joined: |
quote: ********************************************************** Ah Peter, resorting to personal attacks on my and SLPx integrity as reviewers to further your agenda? I reject papers when the data is bad or the conclusions are not supported by the data. I don't reject papers because an author has a different opionion than I do. I would actually think from your postings that you would be more likely to indescriminatley reject papers that conflict with your religious worldview regardless of the science behind them. CiaoM
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derwood Member (Idle past 1876 days) Posts: 1457 Joined: |
Peter the false witness boy:
"BTW, I discussed this already with Dr page himself and he couldn't address it beyong 'maybe it isn't properly rooted'." This is entirely untrue. I have mentioned that I would like ot discuss this, but PB never has, not with me anyway. I have never made such a reply. Peter B has taken the route of the desparate creationist, putting words in the mouth of his opponant (see especially his last post to me!) and engaging in dishgonesty. We should all be wary of this.
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derwood Member (Idle past 1876 days) Posts: 1457 Joined: |
Please not the sections in bold:
quote: Why is it that I have come to expect this sort of thing from Peter B, creationist? Oh, I know - its the whole creationist thing...
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derwood Member (Idle past 1876 days) Posts: 1457 Joined: |
quote: Thanks, Pete. I do find your posts most confusing.quote: You know, it is the strangest thing. Looking at my post #52, I did indeed post a reply to Williams with a link to a Science article containing information on Cairns. But if one looks at the links to replies in the bottom of that post, one sees that you did not respond to it until post #123. This of course is well after I had already reposted a quote from that source and supplied several abstracts to papers that provide direct evidence against 'directed' mutations - the ones you claimed were in fact evidence for them. While I see that I was in error in so far as interpreting your post #123 and #126, I maintain that you did not read, or perhaps understand, the implications of the abstracts I posted in #96. One has to be a dogmatist extraordinaire to believe that papers explaining how mutations occurred genome-wide really indicate a non-random mechanism.quote: Yes, I see that now. My sincere apologies. However, again, I quoted from that article in a message directed to you, to which you responded immediately with some nonsense about the articles really supporting non-random mutation. And again we see that the creationist hangs his hat on what might be, rather than what is.quote: I am wrong? Well, then, Peter B., please supply us with the documentation for non-random mutations occurring in multicellular eukaryotes that result in phenotypic change. The best he could do was some pap about sea gull wings... Which of course had no genetic analysis in its support...Spetner the creationist could not do this then, and he has not done it yet. Help him out. quote: So he was wrong then. Good to hear you say that.quote: I didn't. Indeed, the Cairn's bit was mentioned in regards to "non-random mutation" in general, not to anyone's vanity press book targeting a lay audience.quote: In reality, so many experiments were carried out to see if he was right (he wasn't), not to try to disprove him.quote: What progress would be made by accepting a fringe idea on non-random mutation? I object/deny it because as I have repeatedly explained and supplied references for, the idea of non-randomness is not what it is made out to be by folks like you.quote: They do? Examples please. quote: This is a major misrepresentation on your part, Peter B. It is outright false.Your credibility - what little you may have once had here - is now completely gone. quote: This is just asinine, and indicative of your dogmatic ignorance. Any text on molecular evolution not only explains why discrepencies exist, they actually predict that more will be found.quote: I object to your idiocy, but it won't get me anywhere. Is it a 'trick'? That sounds awfully inflammatory, Peter B. Perhaps you don't understand statistics? Or maybe the workings of genomes? Well, either way, your claims are getting more and more bizarre and more and more desparate.quote: The abstract: "The processes of gene duplication, loss, and lineagesorting can result in incongruence between the phylogenies of genes and those of species. This incongruence complicates the task of inferring the latter from the former. We describe the use of reconciled trees to reconstruct the history of a gene tree with respect to a species tree. Reconciled trees allow the history of the gene tree to be visualized and also quantify the relationship between the two trees. The cost of a reconciled tree is the total number of duplications and gene losses required to reconcile a gene tree with its species tree. We describe the use of heuristic searches to find the species tree which yields the reconciled tree with the lowest cost. This method can be used to infer species trees from one or more gene trees." Whats your point? I am constantly amazed at how the creationist interprets 'explanations' as 'excuses' and the like. Pitiful, really.quote: No, it is a valid conclusion.quote: So?quote: What genes might be present in humans but not in man, I wonder...quote: I see...quote: What do you mean sub-population?quote: I don't know about that particular gene, but Paabo's group has done an extensive study on the mitochondrial genome and, why, it must be a mere coincidence, the findings fit wquite nicely with evolutionary hypotheses.quote: I am still waiting for your hypothesis...A response to what? Let me guess - that falsifies evolution too?
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peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
Dear SLPx,
Yes, Mister SLPx, these postions are NOT under selective constraint and are per definition neutral. I guess, mister Futuyma forgot about this, I don't. Why don't you just simply address my comments in a scientific way and try to convince me, instaed of repeating that I am a creationist. I am always open for good scientific arguments. best wishes [This message has been edited by peter borger, 10-02-2002]
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peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
Dear SLPx,
I referred to Roderick Page, the author of "Molecular Evolution, A Phylogenetic Approach".Sorry for confusing you. I mentioned that I --before registration to this board-- I had a lot of private conversations with evolutionary biologists. As soon as I mentioned the current problems in evolution theory and demonstrated this with examples from literature, there was silence. So I know what I'm talking about. Best wishes,peter
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peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
Dear Mammuthus,
If you feel offended: Sorry for that. It happens to me a lot. Try to be a stoic, that helps. And thanks for clearing things and for your comments on the hypothesis. I will take them in consideration. The more scientific comments the better. Best wishesPeter
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peter borger Member (Idle past 7665 days) Posts: 965 From: australia Joined: |
dear SLPx,
In response to your comments on my previous mail: You say:Thanks, Pete. I do find your posts most confusing. I say:That is because it involves thinking beyond the current paradigm. You say:You know, it is the strangest thing. Looking at my post #52, I did indeed post a reply to Williams with a link to a Science article containing information on Cairns. But if one looks at the links to replies in the bottom of that post, one sees that you did not respond to it until post #123. This of course is well after I had already reposted a quote from that source and supplied several abstracts to papers that provide direct evidence against 'directed' mutations - the ones you claimed were in fact evidence for them. I say:Thanks for admitting you were wrong. I agree on the other mail. You say:While I see that I was in error in so far as interpreting your post #123 and #126, I maintain that you did not read, or perhaps understand, the implications of the abstracts I posted in #96. One has to be a dogmatist extraordinaire to believe that papers explaining how mutations occurred genome-wide really indicate a non-random mechanism. I say:I know the implications, and I just wait and see for more experiments on the 'hot' regions. You say:Yes, I see that now. My sincere apologies. I say:Accepted You say:I am wrong? Well, then, Peter B., please supply us with the documentation for non-random mutations occurring in multicellular eukaryotes that result in phenotypic change. The best he could do was some pap about sea gull wings... Which of course had no genetic analysis in its support... Spetner the creationist could not do this then, and he has not done it yet. Help him out. I say:I already helped him out by showing some interesing examples of non-random mutation (although they are not accepted by some evolutionists, including yourself). So, more research in this particular area will be revealing. I predict: Within 10 years non-random mutations will have their place in NDT. my quote:-------------------------------------------------------------------------------- THAT THE MECHANISM IS NOT EXACTLY AS HE (AND CAIRNS) THOUGHT IT WAS, IS NOT SURPRISING SINCE NOTHING IN BIOLOGY IS AS WE EXPECT IT TO BE. -------------------------------------------------------------------------------- So he was wrong then. Good to hear you say that. I say:The original proposal was false. I just wait and see what the hot regions imply. Maybe it implies an indirect mechanism. my quote:-------------------------------------------------------------------------------- FURTHERMORE, THE CAIRNS INTERPRETATION IS ONLY A MINOR POINT IN SPETNER'S BOOK SO YOU CANNOT REJECT HIS ENTIRE BOOK ON CAIRN'S PARTIAL RECANTATION. -------------------------------------------------------------------------------- you say:I didn't. Indeed, the Cairn's bit was mentioned in regards to "non-random mutation" in general, not to anyone's vanity press book targeting a lay audience. I say:At least somebody who tries to educate the lay audience in an anti-nihilistic way. My objections to the hype are all the extrapolations from it. That is, the BullS..T I hear on the television and read in the papers. You --as a respectable scientist-- should also object to that. quote:-------------------------------------------------------------------------------- BETTER READ HIS BOOK INSTEAD OF ONLY HIS OPPONENTS. AND WHY DO YOU THINK THERE HAVE BEEN CARRIED OUT SO MANY EXPERIMENTS TO FALSIFY CAIRNS INTERPRETATION? -------------------------------------------------------------------------------- In reality, so many experiments were carried out to see if he was right (he wasn't), not to try to disprove him. I say:Maybe they didn't perform the right experiments yet. I think a lot more is going on in this operon than we think there is. And what about the cryptic genes? The distinct stopcodons alternated by sense DNA are nor merely for show. I persist, there is a mechanism that can drain this well, and it will be found. Maybe it cannot be found in the laboratory. Maybe one has to look in subpopulations of extant organisms. my quote:-------------------------------------------------------------------------------- THE NDT WOULD HAVE FALLEN, AND THAT IS EXACTLY WHY YOU OBJECT/DENY THE NON-RANDOMNESS OF MUTATION IN THE 1G5 GENE. AND THAT'S WHY NDT BLOCKS SCIENTIFIC PROGRESS. -------------------------------------------------------------------------------- You say:What progress would be made by accepting a fringe idea on non-random mutation? I object/deny it because as I have repeatedly explained and supplied references for, the idea of non-randomness is not what it is made out to be by folks like you. I say:I said this with the 1G5 gene in mind. Denial of observations does not bring science any further. You say (about reconsiliation of gene and species trees):They do? Examples please. I gave you the IL1-beta incongruence. One should be sufficient. my quote:-------------------------------------------------------------------------------- ACCORDING TO EVOLUTIONARY BIOLOGISTS, GENE TREES HAVE TO BE IN AGREEMENT WITH SPECIES TREES. -------------------------------------------------------------------------------- you say: This is a major misrepresentation on your part, Peter B. It is outright false. I say:Please elaborate a bit on it. References etc. You say:Your credibility - what little you may have once had here - is now completely gone. I say:My credibility within the evolutionary community is about zero, I guess. But, so what, I go for truth, not for 'evolutionisms just-so stories'. my quote:-------------------------------------------------------------------------------- WHY? OTHERWISE ALL GENES LYING OUT PROVIDE FALSIFICATIONS OF COMMON DESCENT. -------------------------------------------------------------------------------- you say:This is just asinine, and indicative of your dogmatic ignorance. Any text on molecular evolution not only explains why discrepencies exist, they actually predict that more will be found. I say:Listen Mr SLPx, I don't adhere any dogma's. I just stand up against nihilism. And as I see it, molecular genetics points in the direction of 'creatons interacting with matter in a morphogenetic field'. And you have to present pretty strong arguments to convince me of the opposite. And now I am curious what the hype has invented now to predict discrepancies. So, explain plus references please. (BTW, "to predict discrepancies". Hear what you are implying: 'our hype predicts that phenomenon X may be found and otherwise the opposite of X may also be found.' I call that HUMBUG) my quote:-------------------------------------------------------------------------------- YOU CAN FIND THIS HIGHLY DISPUTABLE MATHEMATHICAL TRICK FOR INSTANCE IN 'MOLECULAR EVOLUTION, A PHYLOGENTIC APPROACH by R. PAGE'. WHAT EVO’S DO IS THE OTHER WAY AROUND REASONING. THEY CLAIM THAT SINCE EVOLUTION IS TRUE, THE EVIDENCE FOR PUTATIVE DUPLICATIONS IS SIMPLY THE INCONGRUENCE BETWEEN THE GENE AND THE SPECIES TREE. I OBJECT TO SUCH SIMPLISICISM. -------------------------------------------------------------------------------- I object to your idiocy, but it won't get me anywhere. Is it a 'trick'? That sounds awfully inflammatory, Peter B. Perhaps you don't understand statistics? I say:No, your are not going to hide behind statistics. That's another trick to not answer. Besides, statistics has nothing to do with putative duplications that are not present. you say:Or maybe the workings of genomes? Well, either way, your claims are getting more and more bizarre and more and more desparate. I say:That the claims seem bizarre is due to the shortcomings of evolutionism on the level of the genome. my quote:-------------------------------------------------------------------------------- FOR EXAMPLES: (http://taxonomy.zoology.gla.ac.uk/rod/papers/page97mpe.pdf). -------------------------------------------------------------------------------- The abstract: "The processes of gene duplication, loss, and lineagesorting can result in incongruence between the phylogenies of genes and those of species. This incongruence complicates the task of inferring the latter from the former. We describe the use of reconciled trees to reconstruct the history of a gene tree with respect to a species tree. Reconciled trees allow the history of the gene tree to be visualized and also quantify the relationship between the two trees. The cost of a reconciled tree is the total number of duplications and gene losses required to reconcile a gene tree with its species tree. We describe the use of heuristic searches to find the species tree which yields the reconciled tree with the lowest cost. This method can be used to infer species trees from one or more gene trees." you say:Whats your point? I say:My point was the incongruence of the IL-1beta family and the absence of the duplication. The only putative duplication to be found in this region is the one that gave rise to human IL-1alpha. Maybe reread my point. And I am not the desperate one. You say:I am constantly amazed at how the creationist interprets 'explanations' as 'excuses' and the like. Pitiful, really. I say:Better try to convince me with a scientific explanation instead of these evo-blahblah. quote: I say:Here you demonstrate again your condescending (dumb and dumber, remember) overconfinced attitude. -------------------------------------------------------------------------------- You say:No, it is a valid conclusion. I say:Based on what? Could you please lead me through your thoughts and how you draw such conclusions. quote:--------------------------------- peter borger writes: THE MOLECULAR GENAEOLGY OF INTERLEUKIN-1-beta demonstrates an aberration from the species tree. you say:So? I say:Why did you cut of this falsification of common decent. It was the quintessence. Maybe you could respond to it in a scientific way. quote:---------------------------------------------------------------------- And concerning the Uebermensch: you were the one that introduced space-aliens to explain genes in humans not present in apes. I can think of several better 'scientific' non-testable explanations. ---------------------------------------------------------------------- I did no such thing. Please stop misrepresenting me and trying to erect straw man arguments. MY RESPONSE;YES, YOU DID. IN RESPONSE TO THE GENES PRESENT IN HUMAN NOT PRSENT IN MAN. -------------------------------------------------------------------------------- What genes might be present in humans but not in man, I wonder... I say:Obviously, you have a very selective memory. The gene in the LCR16a segment: present in human not in apes. You say:How do you propose this comparison be done? MY RESPONSE:AS DEMONSTRATED FOR THE 1G5 GENES IN A LARGE AMOUNT OF SUBPOPULATIONS. --------------------------------------------------------------------------------You say: What do you mean sub-population? I say:Remember the Ig5 gene and the peculiar results that gave when the authors compared subpopulations. That's where my discussion started 3 months ago. quote:-------------------------------------------------------------------------------- I AM INTERESTED IN THE SEQUENCES OF ONE PARTICULARE GENE (SAY HEMOGLOBIN OR CYTOCHROME C) THROUGHOUT THE DIFFERENT HUMAN SUBPOPULATIONS. I WONDER WHETHER THESE DATA ARE PRESENT INLITERATURE? -------------------------------------------------------------------------------- You say:I don't know about that particular gene, but Paabo's group has done an extensive study on the mitochondrial genome and, why, it must be a mere coincidence, the findings fit wquite nicely with evolutionary hypotheses. I say:Is this really your response? Could you give me the references of Paabo studies. Was it caried out in subpopulations. And you write:"I wonder what your more knowledgible and rational colleagues would think if they knew that you were writing - and apparently believe - something so asinine?" I say:Nice try to stop me from doing. My colleagues like new ideas. Ye, why not publish somewhere that i'm an ass. That would be fun, isn't ist. You could join Schrafinator's club. You say:I guess you didn't realize that all those duplicated genes actually fit quite well within an evolutionary framework? I say:And this shows your lack of knowledge on the topic. Once more for you: There is NO association between genetic redundancies and gene duplications. So how exactly does it fit in? Please explain, and send a letter to Nature, since you are the first one. quote:---------------------------------------------------------------------- (ever heard of the second DNA associated code of transcription? And there may even be a third code involved in coactivation of transcription. Firstly, there is NO evolutionary explanation for the first code. And now we find that the first code gives rise to a second code through possible another code. So you better present a pretty good story to explain this by a random mechanism). ---------------------------------------------------------------------- Frankly, no, I have not heard of this. Please provide some verifiable documentation that I can check to see if your depiction of this is accurate. MY RESPONSE:I ALREADY GAVE THE REFERENCES. I AM WAITING FOR A REPONSE. -------------------------------------------------------------------------------- You say:I am still waiting for your hypothesis... I say:You could have found it if you actually were reading my posts. You also say:A response to what? I say:It once more demonstrates your lack of knowledge on contemporary biology. Notably it was published in Science 2001. Everybody reads Science! Except ostriches, I guess. Best wishes,Peter
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Dr_Tazimus_maximus Member (Idle past 3217 days) Posts: 402 From: Gaithersburg, MD, USA Joined: |
Hi Peter, the largest problem with your statements concerning mutation and randomness appear to me to be a confusion with respect to: 1) randomness with an equal probability of a specific occurance over the range of possibilities, 2) randomness with a non-equal proability of a specific occurance over a range of possibilities, 3) and a non-random occurance of a specific possibility over a range. I am sure that there is a better statistical means of saying this, my stats are self taught although sufficient to compile, analyze and submit clinical and production data through the FDA. NDS deals with the second, not the first as you seem to be indicating. In fact, every reference that you have pointed out supports this treatment of the results far more than number 3 (your apparent approach). The Science paper on Histones, which I had on hand, is very supportive of this interpretation as well. The higher rate of mutations in actively transcribing genes has been well known for years. The fact that both the primary and secondary structure of genes play a role in the probability of a mutational event at those sites is also well known. The mutational frequency that everyone talks about is an average of the much higher probability sites and the much lower probability sites. Your directed mutation seems to me to be nothing more than the increased probability based on structural features and is therefor not in conflict with NDS at all.
------------------"Chance favors the prepared mind." L. Pasteur Taz
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derwood Member (Idle past 1876 days) Posts: 1457 Joined: |
quote: Yes, of course. Because after all, the dogmatic evolutionists are afraid to discuss the falsifications of their pet theory. I rather believe that when it became clear that you were not really intereste din any rational discourse - as one can see form your TalkOrigins feedback and your posts here - that they decided to stop wasting time on you.
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derwood Member (Idle past 1876 days) Posts: 1457 Joined: |
quote: Odd - this does not even address what I wrote. YOU wrote that Kimura claimed this and that, then later admiotted that it was what YOU had in mind. I simply demonstrated the inconsistency, Mr.Borger.
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