molecular genetic proof against random mutation (1)

SLPxOK. Thanks for that clarificaiton. It sounds like Fred was overstating a pet theory of his and would probably admit that now (he seems to in his recent post). Hopefully we can all look at it as a proposal that now needs evidence.I think you know my stance - I think it was primarily standard NDT/microevoltuion/mutaitons/natural selction - whatever you want to call it. For me the large amount of it is probably due to the radiation during the flood.

FredThanks for qualifying your viewpoint.I agree with the dead obviousness of evidence of design.For me the extent to whcih adaptive mutaitons invalidates microevolutionary NDT is dependent on the extent of adaptive mutations. I have to admit that I cannot conceive of an inherent mechanism for adaptive mutations. I can conceive of 'built in' mechanisms for adaptive mutations (I thik my cone-shell example is one) and this would need to be demostrated in the lab to be widespread. This really should not be that hard to do in standard virology labs.Thanks for the fill in on Haldane etc.I see your point from the creaitonist POV - what's wrong with radiation induced mutations during the flood? Is this irrelevant becasue Haldane's result show the limiting parameter is number of generations? I would suggest that Haldanes assumptions need to be very carefully checked.OK so you can see high mutation rates + founder effect + genetic drift can account for the diversity we see since the flood.OK so Haldane required a certain anount of 'beneficial mutaions'. How did he measure/quantiate that?I find your point interesting that drift/selection may not actually work for long-termevoltuion. It is possible and perhaps the appropriate simualtions have not been done. Using Haldane's formalism could be a good start. Are you doing this? (I'm not suggesting you do - there are more important things in life too. ) It is quite possible that one could show that in addition to getting short term imporvements and fittness one also gets long term decay. I am right with you on that and that work should be done my someone. I agree with the evoltuionary POV that it must occur in large populations but the simualtions could still rule it out.Yes I mean mean micro-evolution through allopatric speciation.OK - thanks for clearing that up.It seems to me that you might have overly frustrated SLPx (is that Scott is it?) by overly stresssing adaptive mutations?Good luck with the CRS web site.My main point is that random mutations definitely generate at least short term improvements in fittness in real life examples (bacteria etc). I have no doubt it works in nature too. Yes, whether it works long term (without causing extinction) is a good question. How it relates to post-flood diversity is of course an important point but I don't see obvious problems with random mutations doing it with the proviso that I have not studied Haldane etc. I personally doubt that adapative mutations will be the answer but I welcome surprises in science.

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[This message has been edited by Tranquility Base, 07-18-2002]

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Originally posted by peter borger:
If you like I'll show you how to falsify natural selection. Better admit that NDT has fallen.
Peter

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Please do.

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Originally posted by Fred Williams:

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It sounds like we are both being tripped up by the other’s view of what NDT is. I agree that random mutations occur, and that selection works as a conservation mechanism to preserve the species. But this isn’t NDT. NDT argues that random mutation/selection is the mechanism that has taken a cell to a fish to a frog to a man. NDT therefore requires the existence of beneficial mutations that add or increase the information in the genome.

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Does a fish contain more information than a frog (or a man) in
your opinion (and under your definition(s) of information
content in critters) ?[Added by edit]Just re-read this and Fred does say 'add or increase' so that
answers my question I think. Sorry.

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[This message has been edited by Peter, 07-23-2002]

Is it possible that genetic repair mechanisms could
'partially' repair a copying error ?That is not completely correct the copy error, but
mitigate it so that a functional protein 'close' to
the original is formed.Just a thought ... I'm not a micro-biologist

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Originally posted by Fred Williams:
Citation please.

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Sure - when you provide citations for your claims.

Oh, what the heck:Cairns Excerpt[Fixed and shortened broken link. --Admin]"The flurry of studies ultimately revealed that Cairns's original proposal was untenable, and the community, including Cairns, now at the Radcliffe Infirmary in Oxford, United Kingdom, discarded it."There was another article in which Cairns was interviewed and admitted that his original conslusions were unwarranted, but I have been unable to find it. Nevertheless, as indicated in the above quote, he has 'discarded' his original proposal.

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[This message has been edited by Admin, 07-20-2002]

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I agree with the dead obviousness of evidence of design.

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It used to be dead obvious that the Earth was flat.

Dear SLXYou write that:
"At the OCW board, for over a year, you were asked to support your repeated mantras on this issue, and you never provided a single shred of evidence. On the other hand, I and others provided literally DOZENS of citations demonstrating that what the creationist hawks as 'directed mutation' (ala Spetner) are in fact genome-wide hypermutations resulting from oxidative stress. They were not 'directed' at any specific sites. Indeed, the 'discoverer' of the phenomenon, Cairns, after whom the phenomenon was sometimes called, retracted his original conclusions after seeing additional data."I wonder how these data were obtained? Did the authors compare within or between (sub)species? I will affect the outcome. Could you provide me with the references and the sequences that were compared.
I expect DNA damage induced by oxydative stress to be random, since it is expected from oxygen radicals to act randomly. In contrast, mutations in response to the environment may be non-random and involve protein mediated (a) mechanism(s). We know of one mutation generating mechanism involved in antibody improvement. It is thought of as random. However, nobody has had a very close look at it to come to conclusive evidence. It maybe even non-random. I expect it to be non-random since it is protein mediated.
Peter

SLPx's link is to an article at the AAAS site for Science Magazine, a journal of science whose personal subscription price of $150/year puts it out of reach of most individuals, and whose institutional subscription price of $500/year puts it out of reach of most public libraries. This makes this journal inaccessible to most people, but if there's interest in the full text of any Science Magazine article then it can be made available here at EvC Forum. A mirror of this article, titled Can Organisms Speed Their Own Evolution?, has been placed on site.--------------------EvC Forum Administrator

Dear Admin,
Could you please provide the reference. I have access to Science Magazine. Thanks in advance,
Peter

At the bottom of article, of which Admin suplied the link to, is:
Volume 292, Number 5523, Issue of 8 Jun 2001, pp. 1824-1827.Moose

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[This message has been edited by minnemooseus, 07-21-2002]

PeterWhat you ahve suggested sortof happens in one way in the standard understanding. Each amino-acid is ocded by mulitple codons. Many DNA mutaitons do nt change the protein one bit! Some of them maintain a similar amino-acid. The genetic code has been found to be near-optimal at doing this. I personally doubt that anything detailed using repair enzymes could occur to improve on this further.Again let me point out that it is 3D folded protien shapes that makes the world go around and the concept that the cell had some system of predicting this shape from DNA sequence really does seem like science fiction. Limited preprogrammed egs like antibodies and my cone-shell example are a different beast than some intrinsic systematic Lamarkian mechanism.

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I see your point from the creaitonist POV - what's wrong with radiation induced mutations during the flood?

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Regardless of the amount of radiation during the flood, the starting pair would still have at most 4 alleles per locus between them (sure, the animals in sevens would have more). Any radiation event that would have any significance toward diversity would have to occur several generations after the flood.

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Is this irrelevant becasue Haldane's result show the limiting parameter is number of generations?

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The true limiting parameter is the reproductive capacity of the animal. A new allele can go from few to many only so fast, and this rate is governed by how many offspring the parents can produce in their lifetime. A certain percentage of offspring are going to suffer genetic death (via sickness, rock falling on head, being a prude, etc). The remaining offspring are available to pass on new traits.Note that Haldane’s problem pertains to the spread of beneficial mutations, something required by evolution and not by creation. So, while radiating local populations (demes) might do the trick for the creation model, it actually makes matters worse for the evolution model because the cost of harmful mutation increases.

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OK so Haldane required a certain anount of 'beneficial mutaions'. How did he measure/quantiate that?

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Haldane didn’t make statements that I know of pertaining to some required number of mutations under positive selection required for evolution.

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Using Haldane's formalism could be a good start. Are you doing this?

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To a certain degree. Something that falls out of Haldane’s model is the cost of harmful mutations. I wrote an article on this: http://www.evolutionfairytale.com/articles_debates/mutation_rate.htmTo summarize, using the most recent data we find that each breeding couple since the simian/man split would have had to produce an average of 60 offspring just to maintain genetic equilibrium in the population! This is hard evidence against chimp/man shared ancestry. Evolutionists have no answer for this other than the just-so story of strong epistasis/truncation selection (I discuss these in the article). Note that my article need not rely on the validity of Haldane’s substitution cost.(another note: I wrote the article shortly before the gene count studies that reduced the estimate to ~30K; Regardless, recent studies show the problem is worse than when I first wrote of this; see addendum at bottom of article).

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It seems to me that you might have overly frustrated SLPx (is that Scott is it?) by overly stresssing adaptive mutations?

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I never "overly stressed" adaptive mutations. Scott has made it appear to be a BIG issue to me, when in fact it never has been. When we first debated Haldane’s Dilemma, I freely acknowledged it could be a problem for YEC, and suggested that one possible solution (among others) was adaptive mutations because they represent such a clean, one-generation fix. I did not hang my hat on adaptive mutation, though I did feel (and still do) that there is mounting evidence for it. Where clear misrepresentation crops in is when he claims I said 'large and growing cache of evidence'. This is embellishment, I never thought there was large evidence. I do NOT believe the evidence is overwhelming, not even close, and I expressed this then (which Scott apparently forgot). I admit I can understand how someone might misconstrue mounting evidence with large evidence, but there is a difference. Anyway, for the last few months Scott has been chasing me around with this pseudo-strawman of his, trying to get me to debate him on it.As a reminder, when I first popped in to this thread my purpose was not defend the Peter’s evidence for adaptive mutation. My initial intent was merely to defend Peter’s claim that their existence indeed invalidates NDT, and I cited a leading evolutionist to show this.

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My main point is that random mutations definitely generate at least short term improvements in fittness in real life examples (bacteria etc). I have no doubt it works in nature too. Yes, whether it works long term (without causing extinction) is a good question.

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But even evolutionists acknowledge that in the vast majority of cases the wild-type is still more viable than the mutated strain that developed resistance through a random mutation. Evolutionists are always very hard-pressed to present compelling evidence where the mutated type is superior to the wild-type. I am aware of examples where the evolved strains develop compensatory mutations; but these mutations appear to only have positive selective value with already-debilitated drug-resistant strains. BTW, these compensatory mutations ironically provide indirect evidence for non-random mutation. For example, see: http://www.pnas.org/cgi/content/abstract/95/7/3949?ijkey=uy2u8EdSMiAIQNote the AAC-AGA mutation and it’s implications for adaptive mutation. Evidence? Yes. Proof? No.Gotta run. My time may be limited in the near future.

As far as I can tell, Cairns is still feuding with Rosenberg et all that these mutations are happening in a non-Neo Darwinian fashion. See: http://www.genetics.org/cgi/content/full/156/2/923?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=Cairns&searchid=1027378300880_2030&stored_search=&FIRSTINDEX=0&journalcode=genet icsApparently there is something about Cairns original proposal that he no longer holds to. However, Cairns doesn’t accept the idea that only a small subpopulation is being hyper-mutated, and that is how Rsoenberg et al are able to make the claim that the mutations are random as required by NDT.