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

Dr Page, you've done it again! After reading your stuff, I literally laughed my pants off! You've chosen the wrong job. You could be a comediant. More (obliterative comments) soon.Best wishes and a happy NY,
Peter

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 ... ?

Dear Peter,I will soon eleborate on the mechanisms involved in non-random mutations, but that will take a bit of time. The hotspot mutations in p53 mentioned earlier on this board were already hinting in the right direction. If you wanna know all ins and outs of non-random mutations, I recommend you to read Lynn Caporale's book "Darwin in the genome". I've read it over the weekend and it is more compelling evidence for non-random mutations. Her book also provides molecular mechanisms that explain these particular type of mutations and can even explain recurring indel-mutations. As I claimed before, it is also possible to predict non-random mutations. That is, the position where they are going to be introduced, and the nucleotides involved. It is definitely the end of the NDT era. Also, they have far reaching consequences for molecular phylogeny. Orthodox evolutionists will not like it (and that's an euphemism).Best wishes,
Peter

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Originally posted by peter borger:
Dr Page, you've done it again! After reading your stuff, I literally laughed my pants off! You've chosen the wrong job. You could be a comediant.

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More (obliterative comments) soon.

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Best wishes and a happy NY,
Peter

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Yes, replying to your disjointed, megalomanical rants does tend to be comedy-prone.
I was especially tickled by the fact that you don't seem to know that humans and chimps are in the same Class....[This message has been edited by SLPx, 01-06-2003]

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Originally posted by peter borger:
Also, they have far reaching consequences for molecular phylogeny. Orthodox evolutionists will not like it (and that's an euphemism).

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It will be interesting to see the explanations for how these "non-random mutations" - the ones that are not so non-random as to appear random, anyway - produce phylogenies that just happen to be largely congruent with phylogenies not based on molecules.It will also be interesting to read the explanations for how non-random mutations produced tree topologies that reflected known phylogenies.
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Science 1992 Jan 31;255(5044):589-92Experimental phylogenetics: generation of a known phylogeny.Hillis DM, Bull JJ, White ME, Badgett MR, Molineux IJ.Department of Zoology, University of Texas, Austin 78712.Although methods of phylogenetic estimation are used routinely in comparative biology, direct tests of these methods are hampered by the lack of known phylogenies. Here a system based on serial propagation of bacteriophage T7 in the presence of a mutagen was used to create the first completely known phylogeny. Restriction-site maps of the terminal lineages were used to infer the evolutionary history of the experimental lines for comparison to the known history and actual ancestors. The five methods used to reconstruct branching pattern all predicted the correct topology but varied in their predictions of branch lengths; one method also predicts ancestral restriction maps and was found to be greater than 98 percent accurate.
*******************Science 1991 Oct 25;254(5031):554-8Gene trees and the origins of inbred strains of mice.Atchley WR, Fitch WM.Department of Genetics, North Carolina State University, Raleigh 27695.Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.Phylogenons, anyone?Oh and please - keep your pants on this time.

Dear Page,Page: I was especially tickled by the fact that you don't seem to know that humans and chimps are in the same Class....PB: I recall somebody (Goodman?) claiming them to be the same species.best wishes,
Peter

quote:

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Originally posted by peter borger:
Dear Page,

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Page: I was especially tickled by the fact that you don't seem to know that humans and chimps are in the same Class....

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PB: I recall somebody (Goodman?) claiming them to be the same species.

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best wishes,
Peter

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As seems to be par for the course, you "recall" fallaciously.We consider chimps and humans to be of the same Genus due to a uniform application of taxonomic criteria, that being estimated time since divergence.King Philip Came Over For Grass Sandwiches.

Dear Page,Page: We consider chimps and humans to be of the same Genus due to a uniform application of taxonomic criteria, that being estimated time since divergence.PB: homo or pan?Best wishes,
Peter
Peter

dear Page,quote:
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Originally posted by peter borger:
Also, they have far reaching consequences for molecular phylogeny. Orthodox evolutionists will not like it (and that's an euphemism).--------------------------------------------------------------------------------Page: It will be interesting to see the explanations for how these "non-random mutations" - the ones that are not so non-random as to appear random, anyway - produce phylogenies that just happen to be largely congruent with phylogenies not based on molecules.
It will also be interesting to read the explanations for how non-random mutations produced tree topologies that reflected known phylogenies.
******************
Science 1992 Jan 31;255(5044):589-92Experimental phylogenetics: generation of a known phylogeny.Hillis DM, Bull JJ, White ME, Badgett MR, Molineux IJ.Department of Zoology, University of Texas, Austin 78712.Although methods of phylogenetic estimation are used routinely in comparative biology, direct tests of these methods are hampered by the lack of known phylogenies. Here a system based on serial propagation of bacteriophage T7 in the presence of a mutagen was used to create the first completely known phylogeny. Restriction-site maps of the terminal lineages were used to infer the evolutionary history of the experimental lines for comparison to the known history and actual ancestors. The five methods used to reconstruct branching pattern all predicted the correct topology but varied in their predictions of branch lengths; one method also predicts ancestral restriction maps and was found to be greater than 98 percent accurate.
*******************Science 1991 Oct 25;254(5031):554-8Gene trees and the origins of inbred strains of mice.Atchley WR, Fitch WM.Department of Genetics, North Carolina State University, Raleigh 27695.Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.PB: I do NOT object to these observations within ONE species. I expected them anyway from the GUToB. However, the NRM are immediately clear: in the immune system and the viral sites. Both have been decribed in the book by Dr Caporale.
Dramatically, it tells us that viruses cannot be used for phylogenetic analysis! So, the evolutionary common descent interpretations on HERVs and other shared viruses are invalidated by these observations. Too bad, also for Mammuthus (where is he?).Best wishes,
Peter

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.

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

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).

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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?

Dear Peter,P: You appear to be describing an mechanism that is prone to errors
which are introduced at random ... leading us straight back
to random mutations.PB: Random mutations that appear over and over on the same spot are called POSITIONAL NONRANDOM MUTATIONS and will give the illusion of common descent. Hairpins are only formed upon internal complementarity of DNA (=base pairing) and are therefore sequence dependent. So, the mutaions are dependent on DNA sequences (as observed for the nonrandom mutaions in p53). Same 'class' same sequence, same mechanism, same non-random mutation, same shared mutations, NO common descent. Easy as that. Get it?
It will indeed take a bit of time before one is to believe that NDT has fallen, and that molecular common descent may be explained by NRM. But, a fact is a fact, and I can't help it. The one theory comes the other theory goes. That's science.P: I'll try to get hold of a copy of the book you mentioned ... perhaps in the meantime you could summarise the content?PB: Yes, better get a copy and read for yourself.Best wishes,
Peter[This message has been edited by peter borger, 01-08-2003]

So what provokes a non-random mutation?

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.Best wishes,
Peter