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Author | Topic: molecular genetic proof against random mutation (1) | |||||||||||||||||||||||||||
Fred Williams Member (Idle past 4883 days) Posts: 310 From: Broomfield Joined: |
quote: Scott, you are showing your insecurity yet again. Is that what, the 30th time now you've mentioned the funcional vs genic mistake I made over a year ago? Need I remind you of your numerous mistakes, including claiming that SNPs are fixed, and that a fixed mutated allele can still have the wild-type within the population? You are a PhD biologist. What is your excuse again? Oh, and your memory is horrible as usual, since I never once claimed that evos know how to remove SNPs from a single taxon's DNA. It would be greatly appreciated if you would cool it with the blatant misrepresentation. Since you invariably will respond, I suggest you move your comments to the flames section, if there is one here. No need poluting this thread further.
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peter borger Member (Idle past 7692 days) Posts: 965 From: australia Joined: |
dear SLPx,
I invite you to have a very close look at all known sequences of the GLO gene. It mutates non-randomly, implying directed mutation (while it is not even functional!). Maybe this is what you are looking for. I also invite molecular biologists to sequence the GLO gene of the (at least) two primates that still synthesize vitamin C. That would shed light on the issue. Best wishes, Peter
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mark24 Member (Idle past 5222 days) Posts: 3857 From: UK Joined: |
quote: Peter, The statistical definition of "random", as it pertains to nucleotide sequences, is specifically that each site has an equal chance of mutation. Since there are hot spots where the chance of mutation is higher, mutations are therefore non-random where hot-spots exist. However, every site does have a chance of mutation, & you cannot predict where the next mutation will occur, so it is random in that sense. You seem to be claiming that mutations are non-random in the statistical sense, then dropping the statistical definition for a more colloquial one, meaning non-random is deliberate, rather than just not-of-an-equal-chance. You cannot conflate the two definitions to suit yourself. There isn't a random chance that a car of a particular colour will be next to drive down my road, does that therefore infer that a creator is "deciding" what colour car will be next down my street? Mark ------------------Occam's razor is not for shaving with. [This message has been edited by mark24, 07-23-2002]
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Peter Member (Idle past 1506 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
I was wondering about the possibility that while the
occurence of copy errors might be random, that the possible substitutions that occur are not, but are mitigated by the copy-repair mechanism. This seems even more likely in light of the need to foldcorrectly. Could this create a functionally similar protein, yet onethat has an effect on the phenotype. It would still be random in the sense of when and where, butmight have an apparent adaptive feature due to repair.
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derwood Member (Idle past 1903 days) Posts: 1457 Joined: |
quote: ==================================================================In reference to molecular phylogenetics methods: Fred:... When informed evolutionists speak of the difference between chimp and man, they are referring to fixed differences.=== R: "So, here is my question: How do you discern a difference due to fixed mutations from a difference due to accumulating SNP's in 2 respective populations?" Fred: Via molecular analysis. Again, it makes no sense to compare noise (most of which likely represents deterioration) of one species to the noise (deterioration) of another to determine how much they differ. Note that the roughly 2.1 mil SNPs represents only about .07% of the genome.======================================================== Seeing as how such analyses typically deal only with single specimens, as was made perfectly clear to you prior to your making the above statements, it follows that you believe(d) that "genetic analyses" can identify polymorphic sites in a single sequence. If not, then you either: 1. Are ignorant of how phylogenetic analyses are performed (this should not be true as I already indicated, it had been explained to you by more than one person) or 2. Simply refusing to correct your own erroneous information. The only misresentation and pollution appears to be coming from you.
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derwood Member (Idle past 1903 days) Posts: 1457 Joined: |
quote: I concur.
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Admin Director Posts: 13036 From: EvC Forum Joined: Member Rating: 2.1 |
SLPx and Fred Williams:
It is requested that you both find avenues consistent with the Forum Guidelines for expressing the frustration you each feel. ------------------ --EvC Forum Administrator
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derwood Member (Idle past 1903 days) Posts: 1457 Joined: |
quote: I see that WIlliams is still refusing to explain what that measure actually means. Clearly, it sounds like an insurmountable problem - numbers are often employed that way. Is this also 'hard evidence' against within-kind variation that exhibits similar numbers, or just the human-ape question? quote: While I have no intention of rehashing old times, or of engaging Fred the way in which I have in the past, I do feel compelled to respond to his latest charges.Williams claims that he has never claimed that there is a large and growing cache of evidence supportive of so-called directed mutations. Fred is correct. He never wrote (at least that I can find) that there is a large and growing cache of such information. However, such a denial is a mere nitpick, for he has written that there is a growing cache of such information. If this cache has been growing for so loong, surely, by now it must be large. Observe, emphases mine: "But there is a very good explanation, and it is backed by a growing cache of evidence. I've been a proselytizer of it here many times. John Paul has raised this too. Its called NON-RANDOM mutations; that is, environmentally cued, adaptive mutations! Such mutations incur essentially NO reproductive cost." Oh, and this too: Fred:"Creationists have a plausible explanation for rapid diversity in a short period of time that easily handles Haldane Dilemma. Much of the diversity is likely due to 1) bottlenecks and subsequent drift (but certainly nowhere near 24 million fixed mutations, as the substitutional rate argument above shows is not plausible), and 2) many mutations may be due to environmentally cued mutations (thus addressing the rate problem)." Such a terrible, terrible misrepresentation!
quote: Talk about misrepresentation! Asking you to provide a single citation from this 'cache' of evidence - and waiting for over a year for this amazing article you said you were writing on the subject - is hardly trying to get you to debate! What an inflated ego some creationists develop... quote: Shame that you could provide no actual evidence... [This message has been edited by SLPx, 07-23-2002]
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peter borger Member (Idle past 7692 days) Posts: 965 From: australia Joined: |
Dear Mark,
I agree with you on: "The statistical definition of "random", as it pertains to nucleotide sequences, is specifically that each site has an equal chance of mutation." However, I do not agree to"Since there are hot spots where the chance of mutation is higher, mutations are therefore non-random where hot-spots exist. However, every site does have a chance of mutation, & you cannot predict where the next mutation will occur, so it is random in that sense." Because hotspots imply a mechanism. And a mechanism implies involvement of RNA and/or proteins. Besides, I already mailed (somewhere) that at least two mechanism may be implicated in mutation. Firstly, there is a random mechanisms. Probably, the oxydative stress induced mutations is random (I expect this from the random nature of oxygen-radicals). Secondly, there may be a environment directed rearrangement and/or mutation of DNA sequences. Nobody has found the underlying mechanism(s) yet, but that is not so surprising since the major part of the proteins of any organism is still unknown. In my opinion, the mechansims will be hard to elucidate (and that is why they have not been observed yet), because the proteins involved do not have a direct measurable function. You say that:"You seem to be claiming that mutations are non-random in the statistical sense, then dropping the statistical definition for a more colloquial one, meaning non-random is deliberate, rather than just not-of-an-equal-chance." Indeed, since I think there is a (protein and/or RNA mediated) mechanism involved. I do not mean that the mutation has been introduced deliberately on that spot. Because we do not know the undelying mechanism(s) we do not recognize it as non-random. As soon as the mechanisms are elucidated we will recognize it as non-random. As long as these studies are performed between species we will never be able to elucidate the mechanism. What we need to look at is between and within subspecies (as the Drosophila example). That will provide clarity.Similarly, I always wondered why in hematological disorders (leukemia's) often involve exactly the same chromosomal translocations in the same genes and independent of the population. It implies a mechanism. "You cannot conflate the two definitions to suit yourself." I don't. "There isn't a random chance that a car of a particular colour will be next to drive down my road, does that therefore infer that a creator is "deciding" what colour car will be next down my street?" That's not what I mean. I mean that if a non-random mechanism is operable to generate mutations in genes in response to the environemt it makes it hard not to believe in design. Best wishes,Peter
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mark24 Member (Idle past 5222 days) Posts: 3857 From: UK Joined: |
quote: Why? Given we don't understand what causes hotspots, don't you think you are jumping the gun? Mark ------------------Occam's razor is not for shaving with.
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peter borger Member (Idle past 7692 days) Posts: 965 From: australia Joined: |
Dear Mark,
Why are bananas bended? I already mentioned that science is not interested in why-questions, it's metaphysics. As soon as we find out the mechanism underlying hotspots, we can discuss this in more detail. And I am not jumping the gun, that is what evolutionists do. Ever read the "selfish gene"? That is one big jumping-to-conclusion-book. As long as we do not know the DNA molecule, I will object to that. Furthermore I demonstrated that the NDT is not valid at the molecular level. What else do you need to be convinced? Proof against natural selection? I will not give that here, but I recommend you to follow the literature carefully. Best wishes, Peter
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John Inactive Member |
quote: I once recieved a pamplet from a Baptist Church explaining that banana's are bent because that way they fit nicely into our hands. I'm not joking. I wish I had kept the pamplet. ------------------
www.hells-handmaiden.com
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peter borger Member (Idle past 7692 days) Posts: 965 From: australia Joined: |
Dear John,
As a matter of fact bananas are bent by gravity. Cheers, Peter [This message has been edited by peter borger, 07-24-2002]
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John Inactive Member |
quote: I knew there was something wrong with that hand hypothesis... Take care. ------------------
www.hells-handmaiden.com
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Peter Member (Idle past 1506 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
Large chunks of physics aren't applicable at the atomic
level ... does that mean they are wrong ? I think you need to be less reductionist in your approaches. Evolution is a systems problem, and systems have emergentproperties that cannot be directly tied to individual components. I don't actually think that anything you have presented is evidenceagainst NDT. I'd say why, but you'll probably dismiss it as story telling. You keep saying you are going to refute natural selection ... there'sa thread about 'Falsifying NS' so maybe you could put forward your tale there.
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