Dr Page's best example of common descent easily --and better-- explained by the GUToB

I had prepared a point-by-point response to this, but instead
I will ask a question and then suggest my interpretation
(and your post was, after all, just your interpretation of that
data in a manner suited to your theory).Question:: What makes you think the genetic changes happened
more than once?My interpretation would be that the changes represent a branch
of a tree, where some of the species are descended from others.I am probably moulding the data to what I expect happened, but
building up an inheritance seems much more likely than
independtly mutating in the same way at the same spot.It's all interpretation, there is not fact.On the other hand, if we build a tree from this data, and then
are told what the organisms are ... and they appear to be
in the right place from an evolutionary perspective whose
interpretation is supported?

I've just read SLPx's reply (or one of them at least)
and have to ask the same question...That is, given the sequences how do you differentiate between
random and non-random mutations?In the segments given Hsy and Hag differ in only two locations,
and in one of these locations none of the other organisms show
a difference from Hsy.This would suggest that the differences are not the result of
any mechanism (directed or not) since they occur in only one
of the whole group.Likewise if the changes DON'T occur in the same place
across the whole group that would suggest that absence
of a mechanism.

As you didn't respond to my post #13 I#ll ask again ....With the sequences presented there are many cases where
changes do NOT occur in the same places.If there is a mechanism at work wouldn't ALL sequences exhibit
such changes in the same positions ... ?

In your model are there some 'random' and some
'non-random' mutations?In the posted sequences, for example, Lca shows changes
on locations unique from any other, and in one location
has a change to an 'a' instead of a 'c'.This does not show determinism.

quote:

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Originally posted by peter borger:
Dear Peter,

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P: In your model are there some 'random' and some
'non-random' mutations?
In the posted sequences, for example, Lca shows changes
on locations unique from any other, and in one location
has a change to an 'a' instead of a 'c'.

​

This does not show determinism.

​

PB: Such POSITIONAL non-random mutations can be explained by the "folded hairpin model". They arise from imperfect hairpins in the DNA that are able to anneal in such way that during replication a (usually the same) nucleotide is introduced over and over on the same spot. Such mutations contribute to the illusion of common descent. For a visulation of the model see Dr Caporale's book page 38. These mutations have been demonstrated in T4 virus as positional non-random mutations. In T4 the 'imperfectly folded hairpin model' is also able to explain deletion mutations. I would propose a similar mechanism for the single nucleotide deletion in the inactivated GLO gene (vit C synthesis) that lines up in higher primates (as extensively discussed in another thread). So, I propose an alternative naturalistic explanation for this peculiarity independent of common descent. I bet I am right (since evolutionism from microbe to man is false).

​

Best wishes,
Peter

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[This message has been edited by peter borger, 01-08-2003]

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You appear to be describing an mechanism that is prone to errors
which are introduced at random ... leading us straight back
to random mutations.I'll try to get hold of a copy of the book you mentioned ... perhaps
in the meantime you could summarise the content?

So what provokes a non-random mutation?

quote:

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Originally posted by peter borger:
Nonrandom mutations are provoked by the DNA sequence. The DNA sequence may form imperfect folded hairpins due to internal complementarity. See the edited version of my previous mail.

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Best wishes,
Peter

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So any given DNA sequence will always 'suffer' the same mutation?

If the mutations always happen at the same spots, and
are provoked by the DNA sequence, why do we have organisms
with different sequences?

[QUOTE]Originally posted by peter borger: [B][I]Page: Non-random as in being caused/allowed to occur at a certain locus due to physicochemical
properties.As Peter said, that is not deterministic.It seems that you have the consequences mixed up with the impetus.
{/I][/B]PB: Still they are DETERMINED by the DNA sequence. [/QUOTE]If the NRM's that you claim were actually non-random (i.e.
deterministic) then all similar DNA sequences would converge.This is not seen in the example posted.Deterministic, incidentally, means that with the same input
and same processing the output will be the same.

quote:

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Originally posted by peter borger:
It may have far reaching consequences for common descent, as I mentioned before. Think about it: Two archetypes have the same genes = same DNA sequences. Non random mutations will line up and give the impression of common descent, while they are not.

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If they have the same genes, and the process is non-random they
will develop in the same direction and always appear to have the
same genes.If they diverge then the mutational process is not deterministic
(i.e. it is random).

quote:

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Originally posted by peter borger:
This is observed in the ZFY region. In fact, now I realise that the ZFY region is a good region to define archetypes.
quote:

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More detail please (and not just a 'well if you'd read my
previous posts ...' after all context changes meaning).

quote:

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Originally posted by peter borger:

PW: If the NRM's that you claim were actually non-random (i.e.
deterministic) then all similar DNA sequences would converge.

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PB: And they do, isn't it? have a look at the row #1 (Ptr1, chimp) and row #10 (Str, Hylobate? or whatever. Page knows). The position of the mutations and the nucleotide are almost identical. Besides, as mentioned the NRM may also depend on the 3D context of the DNA.

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'Almost identicle' isn't very compelling when claiming a non-random/
deterministic process involved in mutations.

quote:

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Originally posted by peter borger:

PW: This is not seen in the example posted.

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PB: I you start with two identical genes in archetypes and nonrandom mutations acting in concert with the environment the overall effect of shared mutations resemble common descent. However, as reiterated I did not exclude random mutations. So, nonrandom mutaions are punctuated by random mutations. So, it depends on the context of the DNA stretch and environment of the DNA.

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What are you referring to when you say 'in concert with the environment' (i.e. what environment?) ?What is the 'context of the DNA stretch' that has a bearing on
exactly which mutation actually occurs ?When does this mutation occur ? Every cell division ?

quote:

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Originally posted by peter borger:

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PW: Deterministic, incidentally, means that with the same input
and same processing the output will be the same.

​

PB: Depending on the environment. Not a single cell and not a single DNA environment is the same. The overall effect of NRM and RM is the illusion of common descent.

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Again please state clearly what you mean by 'environment' and 'DNA
environment' in the above.By allowing RM aren't you admitting that NDT does in fact
fit nature, but for you there is more to the story ?

quote:

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Originally quoted by Peter Borger:
The sequence of the DNA stretch is the primary determinant, since during replication ssDNA can fold due to basepairing into dsDNA incomplete hairpins. What happens to such stretches of DNA is
dependent on other interactions with other stretches of DNA, proteins, whether or not a mismatch was present, etcetera. As mentioned before, such incomplete hairpins may change basebaring due to
a single random mutation introduced through oxidation, UV, etcetera.
For these (and probably more) reasons, it is unlikely that all DNA stretches line up exactly as you like to have it. If it were exactly as you like to have that you would say: "look they have all exactly the same positional mutation, that proofs common descent!" But, fortunately we have the ZFY region that proofs that my vision is right.

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What you appear to be saying in the above is::i) There are non-determinable factors in the environment which can
affect which bases suffer copy errors.ii) 'Non-random positional mutations' will only occur if there has
been a random mutation such that folding is modfied.Given the above iterpretation of your comments, it appears to
me that what you are actually high-lighting is that there may
be some biochemical repair mechanism at work which mitigates
the negative effect of random mutations.This is good for a more classical evolutionary vision.Further, that these mutations do not 'line up exactly' is
evidence against NRM in the sense that you first phrased it.If there are 'non-random positional mutations' any gene for
a particular 'function' would be identicle. You have pointed
out yourself that this is not the case (broken Vit-C synthesis
for example).

quote:

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Originally quoted by Peter Borger:
PB: Depending on the environment. Not a single cell and not a single DNA environment is the same. The overall effect of NRM and RM is the illusion of common descent.

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If the exact stimulii for the mutation is non-determinable,
or the timing of such stimulii are not, then what you are
talking about is some form of biochemical repair process
(again). The event of a mutation is still random, but it is
mitigated by some other process.If the gene sequences you have pointed out can give the
'illusion of common descent' then they can also give
the 'illusion of common design' ... which is what you seem to
be suggesting in a very convoluted and long-winded way.However, the simple fact that the 'non-random positional mutations'
do NOT always occur at the same positions makes the
phrase inherently suspect.

You say that the failure to line up exactly could
be caused by 'disturbing' nucleotides which have been
introduced at random. However, in the ZFY sequences posted
we have instances of single base substitutions with all
surrounding bases identicle. In the example there have been
no 'insertions' since this would show up as a complete contrast
(ie. everything after the insertion would be different compared to
the same location on another sequence).How long does a sequence have to be for the NRM mechanism to
operate?

So you cannot predict where these imperfect hairpins
will occur based upon sequence, but only infer from
extant mutations that that is where they lie?

Have you posted how NRM explains this? If you have could
you tell me the post otherwise could you explain this
within your framework, please.

How many differences are there between human and chimp
mtDNA ?