The creationist is nothing if not predictable and overconfident...
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Originally posted by Fred Williams:
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Q: Okay, let's rephrase the question - which has as yet not been answered. IF non-random mutations exist, how would they be identified
Easy. See Cairns, Hall, etc. In short, the discovery of mutation(s) that are the result of an adaptive response to some environmental stimuli. Or, mutations that cannot mathematically be attributable to a chance copying mistake in the DNA.
Well, it isn't that easy in reality. The knowledgible creationist knows that Hall's and Cairn's original conclusions were based on 'partial knowledge' (like Haldane's) - further studies indicated that the effewcts seen by Cairns et al. were the result of genome-wide hypermutation in response to oxidative stress.
But why does math come into play here? And why doesn't the creationist EXPLAIN this 'math'?
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Q: If the non-random mutation hypothesis is true, what evidence would we be able to find in support (or to falsify) the idea?
See Rosenberg, et al. A good paper is EVOLVING RESPONSIVELY: ADAPTIVE MUTATION, VOLUME 2, JULY 2001. It’s been over a year so I suspect this paper might be available for free now on the internet. To summarize, Rosenberg claims there is nothing anti-NDT at all about the apparent Lac+ adaptive mutation. She cited data that indicates a sub-population hypermutation occurred which included many unselected mutations within the Lac+ mutants genome, which would be expected if the mutations were behaving in a random, NDT fashion.
So why again is this supportive of non-random mutations?[/quote]
As Page pointed out, Cairns recanted some aspect of his original study, but from recent literature Cairns obviously still holds to adaptive mutation, disputing an important claim of the anti-adaptive mutation crowed that virtually all the mutations are occurring in a hyper-mutating sub-population. See
Contribution of Bacterial Hypermutators to Mutation in Stationary Phase | Genetics | Oxford Academic RSTINDEX=0&journalcode=genet%20ics[/quote]
Has Cairns - or anyone else - observed this phenomenon in multicellular eukaryotes? Or is the continued creationist insistence upon this as a panacea for their mythology a reflection of their naivete?
But I have to wonder how well the creationist read his link:
"These results imply that most single (Lac+) mutants are arising in cells that have a lower mutation rate than the cells that produce double mutants. As Rosche and Foster pointed out,
the most reasonable hypothesis is that all cells are undergoing mutation, but a small minority have a much higher mutation rate. In other words, when there is selection for just a single novel trait, most of the survivors will not be burdened with multiple changes in the rest of their genome."
Not only does that
not sound like a ringing endorsement for the creationist extrapolation on 'non-random mutations', but in fact sounds very Darwinian.
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As for my stand on non-random mutations, see Messages 44, 59 from July in molecular genetic proof against random mutation. To summarize, the primary purpose of my entry into that thread was to defend Peter’s claim that discovery of such mutations falsify the current NDT paradigm, and I provided a quote from leading NDT advocate Dr Futuyma proving it. I stated that I believe there is evidence for non-random mutations, but nothing to hang one’s hat on (Transposons for one have all the appearance of being a non-random, pre-programmed type of mutation).
You have been stating such a 'belief' for some time, and claimed to be writing an 'article' on it as reason not to supply citations supportive of this 'belief' in the past, and this inability to supply supportive documentation has not changed. The mechanisms of insertion are hardly the silver bullet you want. To see if you can figure out why, perhaps you can explain how transposons 'find' an insertion site.
Here is a hint - there is a simple explanation for it.
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I also once believed non-random mutations would explain Haldane’s Dilemma as it applies to rapid diversification since a flood 5K years ago, but backed off this observation as later personal studies of the dilemma demonstrated that rapid diversification could easily occur without the aid of non-random mutations.
"Personal study"? Let me guess - you are writing an 'article' about this for your personal web site and so deign not to grace us with your sound scientific observations - supported with documentation, of course - on this issue.
But that brings up an interesting conundrum - if you think that 'rapid diversification' is possible regardless of Haldane's model, I see no rationale for insisting that human evolution from an ape-like ancestor is untenable.
Care to explain this paradox?
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Page nevertheless continues to quote statements of mine that I have backed off of (messages 44 & 59 are proof of this, in case Page denies I never told him). This is like those dishonest atheists who will use quotes of Abraham Lincoln before he was a Christian in their attempt to show he was not Christian!
What about those dishonest Christians that claim that thsi country was built on Judeo-Christian 'values'?
Anyway, Williams, I like to quote your 'backed off' of statements not to 'misrepresent' you, but to point out your arrogance and hypocrisy.
Did you not at one time insult myself, sumac, and others for daring to disagree with you on SNPs and phylogenetic analysis? Did you not repeatedly claim that "informed evos" (whoever they are - you never did supply a single name!) know that were right, and that we were "morons", "knuckleheads", etc. for not acknowledging yo8ur supreme knowlegde? Only to later (much later) see you claim to have known all along that we were right, and the seeming 'disagreement' was due to the 'shortcomings of the medium' - the medium being written English?
Come on...
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For now, I’m on the sidelines watching the drama play out. I pop into this drama now and then mostly to expose erroneous statements or bad logic like Mamuthus's "good one" in this thread.
Shame that you don't pop in to support your claims, instead of this asinine post-and-run-and-ignore technique that you seem to favor.
So - what is the status of 'information' when:
A gene duplication results in a shift in phenotype?
A mutation results in increased gene expression that provides pesticide resistance?
Or are you going to ignore these scenarios?
You are the 'information theory' expert, are you not? Why not educate all us underlings?
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