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

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Originally posted by peter borger:
dear Page,

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Since you hold a PhD in some sort of science, I expect you to reply in a scientific way.

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Thanks in advance,
Peter

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I take it that you cannot handle the issues brought up by peter and I?

Page,
as soon as I receive your scientific comments that demonstrate where my thinking goes wrong, I will repond to you too, and once more explain my thoughts about this region.I already responded to Peter, how I see the ZFY region and the NRM they contain.Maybe it is time that you get updated with respect to evolutionism: go to the library and get Caporale's book. Try to understand it.
(It can be a bit difficult here and there for outsiders.)In the meantime I will await your reponse.have a nice weekend,Peter

Dear Peter,Thanks for your comments.
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.
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.
--------------------------------------------------------------------------------'Almost identicle' isn't very compelling when claiming a non-random/
deterministic process involved in mutations.PB: Almost identical random mutations in Ptr and Str? You are free to call them random mutations introduced at the same spot. I prefer to describe them as POSITIONAL NONRANDOM MUTAIONS, similar to those described in Caporales book (page 38). Did you already get a copy of her book? It is one of the best I recently read.
The ToE does not even come close explaining this region.quote:
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Originally posted by peter borger:PW: This is not seen in the example posted.
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.
--------------------------------------------------------------------------------P: What are you referring to when you say 'in concert with the environment' (i.e. what environment?) ?PB: The environment of the DNA. The DNA is a huge macromolecule that has millions of interactions with all kind of other molecules.P: What is the 'context of the DNA stretch' that has a bearing on
exactly which mutation actually occurs ?PB: 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 mtation 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.P: When does this mutation occur ? Every cell division ?PB: for more detailed information on when, where, how, you really have to read Dr Caporale's book. But, it is unlike that it happens all the time, otherwise we would see what you expect/wanted to see.quote:
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Originally posted by peter borger: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.
--------------------------------------------------------------------------------P: Again please state clearly what you mean by 'environment' and 'DNA
environment' in the above.PB: Interactions of DNA at the molecular level. As described above, but also depending pH, hydratation, accesory molecules, (an)organic ion-interaction, etcetera.P: By allowing RM aren't you admitting that NDT does in fact
fit nature, but for you there is more to the story ?PB: No, the variation we observe in nature can directly be attributed to such non-random mechanism. It should be clear that NDT cannot. (If NDT cannot even do such minor changes, how can it ever account for the evolution of an organism from scratch? It is a myth!) However, as mentioned several times I do not exclude the possibility of RM, I simply do not believe they play an important role in what you call evolution. Once more, one can not take the one mechanism to extrapolate evolution from microbe to man. If you do, you also have to believe that evolution is mechanistically determined and that is creation.Best wishes,
Peter

I have begun to wonder if the central dogma is not inviolable with the protein back onto DNA (regulation and in hairpins) is not able to return spatially seperated perversion knoweldge base in quartic twist potentials translated back to the original DNA/gene replication govnr +- point mutations by a puncutuational style biology that AIG may have appreciated. Gould may have been able to appreciate this thought but modern biochemsitry seems to have little precedent for engaging in this kind of work on the edge of chaos. As long as there is some other population genetic gene flow in the taxogeny I do not see that the central dogam need stand. Varition in hydrophobic amino acid ratios may accomplish this non-linear dynamic but I do not also see need for the 3 core Darwininsm either. It is not clear that PE itself can survive its own inheritance. THUS mutations can have the effect but we do not seem to have the science able to show this NON RANDOM MUTATION DIVISIONS. I still bet on thermoregulation to yield the tin.Another way to look at this in hind sight is that NRM my show Crick mistaken. This would be my idea of the environment of the DNA in short.

Dear Brad,
Tyanks for your thoughts. I will consider your ideas. Furthermore, Gould is wrong and Crick may be mistaken.O yes, before I forget, Dawkins is always wrong best wishes,
Peter[This message has been edited by peter borger, 01-19-2003]

The way Gould re-framed it was to "trace" conTINental formalism vs anglophonic adaptations. I would not have made the connection to Fisher this way but this does not make GOuld "wrong" in my book. Why do you say he is wrong? Dawkins being correct has however NEVER seemed plausible to me. Obviously data tells more than opinions. I think really it was only that Gould had to deal with Mayr which Croizat rejected offright and onpoint used his birds to his own rate.I did not know about Woods Hole and orthogenesis , but now my converstation with Marjore Green AGAINST Provine makes "perfect" sense and I did not need to win a Golden Globe to agree with Gould.

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.

dear Peter.There are at least three mechanism that introduce NRM. The first mechanism has been described in T4 and depends on the sequence of the DNA stretch that can form imperfect hairpins. These NRMs rely upon DNA repair proteins. The second mechanism is also dependent on DNA sequences for recognition, but -distinct from haipins- are more classical recognition sites present in the genes. Such recognition sites are present in immunoglobulin genes, and T cell receptor genes. Thirdly, there is RNA editing, a mechanism that induced variation through modification of nucleotides in primary transcripts. For instance, certain well-defined C's can be converted into U's, a mechanisms that is also carried out by specific proteins. As you can see, all information for variation is already present in the genome.Best wishes
Peter

dear Peter,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.--------------------------------------------------------------------------------PW: 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.PB: No, I am saying that the NRM spots can be affected by other factors, so that you do not always get a perfect line up of mutations. The fact that the mutations usually do not show perfect alignment is evidence for NRM (as in the GLO gene), rather than common descent.ii) 'Non-random positional mutations' will only occur if there has
been a random mutation such that folding is modfied.PB: No, NRM positional mutations are introduced on the same spot over and over because they are determined by the DNA sequence. Sometimes, this sequence can be disturbed though a random mutations (UV, oxi). The introduction of one disturbing nucleotide will affect the formation of such hairpins. The same holds for other environmental factors, as mentioned in my previous letter.PW: 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.PB: Yes, any organism -even the simplest- have an eleborate DNA repair mechanism. It is the most important thing to propagate the DNA in time. Since genomes are unstable, they tend to disintegrate. So they have to be maintained continuously.PW: This is good for a more classical evolutionary vision.PB: You mean Darwinism?PW: Further, that these mutations do not 'line up exactly' is
evidence against NRM in the sense that you first phrased it.PB: No, it is not evidence against NRM. AS explained several times, as long as mutations are determined by the DNA sequence they are not random.PW: 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).PB: No, since not a single cell is identical, I expect to find deviations from a perfect alignment. That is what we usually see.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.--------------------------------------------------------------------------------PW: 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.PB: I already discussed this. For the positional NRM we do not know WHEN they are introduced, except during replication. My point with the positional NRM is that they line up and give the illusion of common descent. Since NRM cannot be excluded they are the end of the best molecular argument for common descent. It is quite a defeat for evolutionism.PW: 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.PB: Multipurpose genomes have been designed. That is exactly right. Currently they are subject to entropy and disintegrate rapidly. That gives rise to a lot of diseases.PW: However, the simple fact that the 'non-random positional mutations' do NOT always occur at the same positions makes the
phrase inherently suspect.PB: Peter, have an objective look at the ZFY region. It doesn't demonstrate common descent, it demonstrates NRM.Best wishes,
Peter

Isn't it amazing how this "illusion" of common descent in the DNA largely reflects the common dscent inferred from other means?Just one big illusion...

Dear Dr Page,Still waiting for your analysis, Dr Page,Best wishes,
Peter

Dear Dr Page,Page: Isn't it amazing how this "illusion" of common descent in the DNA largely reflects the common dscent inferred from other means?
Just one big illusion...PB: If you can stand another defeat, open a thread and I rebut this one too.Best wishes,
Peter

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?

[deleted double message][This message has been edited by peter borger, 01-22-2003]

Dear Peter,Imperfect hairpins can have variable sizes. The one that has been studied in the T4 virus is 25 nucleotides.
I will look for internal complementarity in the ZFY region soon.Best wishes,
Peter