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

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

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]

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:
--------------------------------------------------------------------------------
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

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

[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

Dear Dr Page,Page: I downloaded the segments form the paper, as well as the entire published human mtDNA genome. Strangely, I have not been able to align any of the human segments from the paper with the mtGenome.
There is one more thing I will try.PB: I think you have a giant publication now, since you are the first that has all complete ancient mtDNA's sequences mentioned in my reference. In other words, don't fool me Page.PAge: As for your "analysis", if you want to call it that, it failed to take certain simple things into account. Stochastic processes, for example.PB: Maybe you could point out what kind analysis you did with these segments and present the precise outcome on this board. I am very interested how you got to this conclusion, since the NRM are quite obvious.Page: Believe it or not, PB, others far more learned than you have taken such things into account.PB: My guess is that they are overlearned; been tought the wrong paradigm and now they try to squeeze in molecular data. Otherwise the teachers will get angry. Biology is quite simple and easy to understand as long as one applies the right paradigm. That is: GUToB.Best wishes,
Peter

Dear Peter,PW: 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?PB: Before you respond to my comments be sure that you know what my comments are about. They are about human ancient mtDNA and the presence of 9 mutations in this region generated over only 62 ky. That is what Page is going to analyse. Apparently he has got a major breakthrough since he has the complete sequences of mtDNA's from all the ancient mitochondria. And now I am very curious, since I claimed that according to the date presented in the reference human and chimp have a common ancestor around 150 ky BP. He is going to falsify that, and now he has these sequences, so I can asure you that is pretty exciting. Furthermore, the fragments showed NRM on 10 positions and that would be similar to the ATP6 gene. I can hardly wait for Page's data analysis.Regarding the hairpins. Since hairpins are internally complementary sequences and can be predicted with an appropriate program. Can alo be done by eye, but that is a tremendously meticulous job. Not preferable.Best wishes,
Peter

Dear Dr Page,PB: quote:
--------------------------------------------------------------------------------Dr.Page: I downloaded the segments form the paper, as well as the entire published human mtDNA genome. Strangely, I have not been able to align any of the human segments from the paper with the mtGenome.
There is one more thing I will try.PB: I think you have a giant publication now, since you are the first that has all complete ancient mtDNA's sequences mentioned in my reference. In other words, don't fool me Page.
--------------------------------------------------------------------------------PAGE: I really do no longer see any reason to reply to you anymore. Any impetus for charity towards you is gone.PB: Listen, Page, you were going to show me and the rest of this board were my analysis went wrong. You simply didn't do that. I can find the complete human mtDNA on internet myself. I claimed that according to the ANCIENT mtDNA data humanand chimp have a common ancestor 150 kY ago and THAT IS WAHT YOU ARE GOING TO SHOW THIS BOARD TO BE WRONG. You don't even come close doing that.You can as well claim that hat you've run a marathon in three hours while nobody was around. SO, SHOW ME YOUR ANALYSIS.PAGE: You are either: Stupid; Dishonest; Incompetent; Being deliberately obtuse; combinations thereof.PB: As mentioned you are nice, polite, charming and eloquent. But NOT a scientist. And above all you are playing bluff poker. If this game we play were russion roulette you would have been dead along time ago.PAGE: I will take you through this slowly, and explain the big words to you, then I am finished with you.Here is what I wrote, important parts are bold:"I downloaded the segments from the paper, as well as the entire published human mtDNA genome."You reply:
"I think you have a giant publication now, since you are the first that has all complete ancient mtDNA's sequences mentioned in my reference."Your twisted, idiotic interpretation of what I wrote is not even close to being excusable, much less explicable, EXCEPT via one of my possible explanations above.PB: Once again for you: YOU WERE GOING TO FALSIFY MY CLAIM THAT CHIMP AND MAN HAVE ACOMMON ANCESTOR AROUND 150 KY BP. YOU AND I KNOW THAT YOU CANNOT DO THAT WITH ONLY THE HUMAN mtDNA, SO YOU HAVE TO DO IT APPLYING WHAT IS KNOWN: THE PUBLISHED SEGMENTS. AND THEY SHOW 9 MUTATIONS OVER 62 KY? DENYING THAT IS DENYING SCIENCE. WHAT KIND OF SCIENTIST ARE YOU?LISTEN CAREFULLY PAGE, YOU MAYBE ABLE TO FOOL THE PUBLIC WITH YOUR CHEEP TRICKS, AND THE OTHER GULLIBLE, BUT YOU CAN'T FOOL ME.I downloaded the SEGMENTS from the cited paper, available here:[Invalid form] - Search Results - PubMedAND the human mtGenome, here:Human mitochondrion, complete genome - Nucleotide - NCBIPAGE: Don't fool you? You ARE a fool.
Even Fred Williams had a redeeming quality (I cannot remember what it is right now).
You seem to be totally lacking.Good bye. For good.PB: Fred wasn't able to push you in a corner, I am.
So, when are you going to leave the board?Good riddance to coarse language.Best wishes, and have a nice rest of your life
Peter