molecular genetic proof against random mutation (1)

Peter BorgerI've read your post but not all of the rebuttals.Can I just say that most YE-creationists (eg myself) would strongly suspect that the various species of Drosophila did diverge from a common anscestor.Why exactly do you doubt that DNA and protein sequences can vary and be selected for? Althoug it took a breakthorgh by Darwin and then the later NDT genetics reformulation it is dead obvious that life MUST work this way. I have seen this with my own eyes in viral evoltuion in the lab. And bacteria can routinely evolve improved enzymes if stressed. There are US companies that are generating enzymes evolved this way for chemical industry!This is not our battleground - our batleground is the origin of distinct kinds.

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[This message has been edited by Tranquility Base, 07-15-2002]

FredForgive my ignorance about NDT etc, but what is the exact problem here? Of course randomness of mutations is part of any sensible genetic theory. It's selection that fits to the environment and makes sequences in organisms both maintain and move to non-random sequences. This doesn't have to violate the design of genomes. Genomes were designed by God but move to non-random nearby positions in seqeunce space via NDT. Are you saying you don't beleive this at a microevoltuionary level? Are their mainstream sceintists who dont' believe this either? From my POV as a molecular biologist it would be impossible for this theory of random mutaiton and no-random selection to not be true! Please enlighten me otherwise!OK, so what you're saying is that there is some evidence of directed mutations or that Futuyama says there is? I have read a little about this and I would personally have no problems with some sort of non-randomness but I would find it hard to beleive that there could be a molecualr mechanism that generate seqeunces that are phenotypically useful systematically. If everybody knew that protein folding/binding is the basis of all of ths they would know what a hard ask this is of course!you say that my optimized enzyme issue violates NDT if it was a non-random mutaiton. The point is it wasn't a non-random mutaiton. It was the one selected from random mutations!Is there anyone on this planet that is suggesting that standard viral evolution in the lab is producing non-random mutaitons (prior to selction)? Please educate me and then either I will educate them or else they have won a Nobel prize if they can prove it.I understand what you are saying but even if there is some bizaree mechanism for non-random mutaitons why would that invaldiate random mutaitons/selection as a mechanism also?OK - I see what you are getting at. The penny has dropped. OK.So you are arguing for a determinstic evolution. Is that what you beleive in? Everything I know about molecular biology argues against this and if you beleive this then you need to show otherwise (I feel like I've heard this from someone before ).I very nmuch disagree with this viewpoint on both scientific and Biblical grounds. But I now understand where you are coming from.OK, now please tell me why you believe this - tell me what this evidence is for non-random mutaitons. I can think of some - I know about low mutation rates of cystines in disulfide bonded cone-shells for example.

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[This message has been edited by Tranquility Base, 07-16-2002]

SLPxI agree that there is no doubt some non-randomness to mutations. It's just very hard to imagine systematic means for generating phenotypiczally useful ones. Such findings are interesting to both evolutionists and creationists but it seems impossible that such findings could change the overall validity of selction from randomness.If I followed what you said then there is evidence that lac mutations correlate over random with those phenotypically successful (why adaptive reversion - do these mutations preferentially go back to pre-used successful mutations?)?My example is of hypermutation of non-cystine codons and lack of mutation in cystine codons is in cone shell toxin peptide genes which are folded by multiple disulfide bridges. At first glance one thinks no surprise - of course the cystine residues must remain cystine residues (due to the disulfide bridges and selection for function). But the point is that the cystine codons do not change (to other cystine codons). A collaborator of mine has reported this work in Science a few years ago and suggests that there must be some molecular mechnism for these particular genes that keeps the cystine codons from mutating. The hypermutaion of non-cystine residues allows the cone-shell toxins to adapt to changing molecular targets in their prey. I have no problem with this but it is clearly a special case (I would of course suggest designed but that is not the point here). Even if such a mechanism were to be found throughout genomes it's not as if it was something inherent but rather molecular systems fine-tuned for each particular phenotypic requirement. It reminds one of how antibody repetoirs work at the gene level - maintinaing a core structure with changing loops. But none of this suggests determinisitic evolution with or without God or that the basic viewpoint of random+selection is undoubtedly the main story.

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[This message has been edited by Tranquility Base, 07-17-2002]

FredI agreew with you about what NDT is - I obviously only expect NDT to do things at a microevolutionary level. The rest I put down to design. For some reason you seem to be wanting to come up with a molecular mechanism for progressive creation? Maybe not - see below.I agree with Futuyama with the proviso of special systems like my cone-shell example (see my last post).Ok, I agree that non-random mutations would probably imply that the information was already coded in the genome some time in the past (just like nmy cone-chell example). Hoever some limited non-randomess (like codon bias etc) is not necessarily evidence of design).My difficulty is understanding why you think non-adaptive mutaions might be so pervasive as well as understanding why you as a YE-creationist are so interested in it. To me the examples so far are Behe type examples of design - fine. But are you tprposing progressive deteminsitic evolution/creaition.I agree with you that random mutations lead to decay but I can also imagine them leading to improvement too (ala the finches). I agree that superimposed on top of small improvements will be a graudal decline. But I would still put Darwin's finches down to random + selection. Remember I have seen this in viral evolution in the lab. the population does get undeniably fitter.My big question: are you proposing that adaptive mutations led to theistic macroevoltuion or are you simply trying to put down finch etc microevoltuion to adaptive mutations?

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[This message has been edited by Tranquility Base, 07-17-2002]

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]

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.