molecular genetic proof against random mutation (1)

I've asked similar questions about linked genes in the
other Peter Borger threads, and he's so far ignored them.

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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

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 fold
correctly.Could this create a functionally similar protein, yet one
that has an effect on the phenotype.It would still be random in the sense of when and where, but
might have an apparent adaptive feature due to repair.

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 emergent
properties that cannot be directly tied to individual
components.I don't actually think that anything you have presented is evidence
against 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's
a thread about 'Falsifying NS' so maybe you could put forward
your tale there.

Sorry to butt in ...

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Originally posted by Philip:
Dear Taz,

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A) Regarding one's quest for proving random mutation, i.e., in mutation spots,

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While I'm amazed at Peter's tenacity to disprove random mutation in certain theorized mutational spots (if you will in my meager understanding), it makes empirical sense to me. For how can the mutation spot possibly be random when it must be determined? Else random mutations (if they were indeed random) would almost always invite detrimental mutations more than beneficial ones (eg. 999 to 1 or whatever). Thus the whole concept of random mutations is a misnomer for determined ones at mutation spots.

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How deterministic vs random are these mutation spots, really Taz?

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I think you may be missing the subtle shift the PB has been using
in terms of randomness.Random for ToE simply means we do not know when a mutation
will occur.The existence of regions of the genome which have a higher
tendency to mutate does not make any actual mutation non-random.It just means that there may be some as yet unknown mechanism involved
when mutations do occur.DNA in the brain cells and immune cells is deliberately
re-arranged in response to dunno-what(in the brain possibly some
memory storage ... New Scientst article on it a while back) and
for immune cells in response to foreign chemicals.Perhaps it's just a hang-on from that mechanism.Doesn't necessarily mean that the mutation is deterministic though,
just governed (perhaps) and by that I mean mechanistically.

quote:

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Originally posted by Philip:

B) Who and how could one assert an organism's consistently occurring gene is non-functional: Are you asking us to believe:
1) We empirically know it has no function whatsoever,
2) That it does not and/or will not react with protein factors, genes, and/or harmones.
3) That its presence is totally arbitrary and expendable in the grand scheme (if you will) of the organism's posterity.
4) That it doesn't even serve as a functional gene-molecule for nucleotide connectivity or other functions.

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Again, this is problem with PB's assertions ... how can you
claim redundancy when you cannot say 100% that a sequence
has no function?Maybe there are 'data' and 'code' regions in DNA????

quote:

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Originally posted by Philip:

In sum, I don't see molecular genetic proof against beneficial random mutation as even necessary to prove that mutation spots must be determined. Such relational determinants must exist (in part at least) to enhance beneficial mutation.

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Again, beneficial random mutation seems a contradiction in terms, regardless of mutation spot characteristics; better phrased I might state them perhaps as: beneficial deterministic mutation.

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My heralding "beneficial deterministic mutation" does not imply complete non-randomization events occurring at the gene level; please don't misunderstand me. I only imply that detrimental mutations are the only truly random mutations.

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I think you lost me here ... or are you still using a different
variation on the term random?Any mutation could be beneficial, non-beneficial, or detrimental
it all depends on expression and how that expression interacts
with the environment surrounding the cell/organism.

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Originally posted by peter borger:

... if an unknown molecular mechanism generates the mutations one can never use this gene to demonstrate common descent. In fact, one cannot use any shared sequence anymore...

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Does this mean you are suggesting that there is a mechanism
which would cause any genetic sequence at a particular locus
to become the same genetic sequence given enough time?Normally one would expect that for a mechanism (or process) to
produce the same output(s), that the initial conditions would
also have to be the same.

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Originally posted by peter borger:

That is something that I wouldn't expect by chance alone.

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This is a strange comment ... what would you expect by chance?If it's 'by chance' pretty much any possible outcome should be
expected, surely.

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Originally posted by peter borger:

If I understand his last sentence properly, he says: "All regions are not equal"

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In my opinion not equal means that a mechanism (=non-random) is involved, isn't it?

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Does this mean that road traffic accidents (RTA's) are directed?There are certain sections of road which are more prone
to accidents than others, therefore the accidents which occur
are not random instances ???????Does that sound like logical reasoning to you?

quote:

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Originally posted by peter borger:
Dear Peter,

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Could yo please elaborate a bit on the road. What kind of road? Where does it wind, become unsealed, is a bar nearby, etcetera. That would shed some light on the cause (mechanism) of the accidents.

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best wishes,
Peter

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The difference which I was attempting (again) to elaborate is
the meaning of 'random' in the context of evolution.Disproving 'random mutation' is not about finding that some
locii are more likely to undergo copy errors. In the same
way that the random nature of RTA's is nothing to do with
black-spots per-se.In an evolutionary context, random means we do not know:When the mutation will occur.
What the mutation will effect/cause in the phenotype.
How that mutation will effect fitness.The higher tendency of some areas to undergo copy errors would
better be described as a chemical property, surely.

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Originally posted by peter borger:

I explained several times now what I understand as non-random mutations (nonrandom with respect to nucleotide and location, you call them hot-spots, I guess).

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Hot spots do not fit the definition of non-random you have
stated above.When a mutation occurs (i.e. a copy error) it may or may not
occur at a hot spot.It is more likely (statistically), but not certain.Your definition would require that the location of any copy error
on any copy can be predicted in advance -- it cannot, to the best
of my knowledge -- and thus is random by the definition of
non-random that you give.

What provokes these non-random mutations?