More non-random evolution

Dear mammuthus,I think that you are a bit confused now. It was Quetzal's question. But anyway, Quetzal will be happy (?) I guess.However, I am aware of these studies and the authors conclude that "three lines of evidence suggest that they [genomic changes] are mostly due to IS-transposition and other types of chromosomal rearrangements. First, [..], point mutations are NOT [caps are mine, PB] abundant in these evolving populations. Second, the extent of genomic change [..] was similar among lines that had become genetic mutators and those that had wild-type point-mutation rates. [..] Finally, we observed significant changes in the copynumber of certain IS-elements [..], most easily explained by transposition and deletion events that produce gains and losses of copies, respectively" (Papdopoulos et al, PNAS 1999, 96:3807)MY RESPONSE:
Thus, although populations change over time, this is not due to the change of nucleotides and therefore not due to changing DNA sequences. The only changes are the ORDER of the sequences, the order of transposable elements and therefore --in my opinion-- gene expression is altered. That is all what is required for distinct phenotypes. No information added or gained. All information was already present. It has been shuffled due to exision and reintegration of DNA through specific proteins (endonucleases, integrases, ligases etcetera). The only thing that was added to the genome in certain cases were additional copies of transposable elements. All this after 10.000 generations! This is NO evolution, it is VARIATION INDUCTION generated by a genetic mechanism already present in the original cells. Similar observations have been done in Enterococcus (Nature 2002, 13 june), that is able to actively shuffle genes on a DNA island in response to antibiotics. Apparently, bacteria have a very plastic genome.
It perfectly fits in the multipurpose genome hypothesis.best wishes,
Peter[This message has been edited by peter borger, 10-15-2002][This message has been edited by peter borger, 10-15-2002]

Dear Quetzal,Today i will reply briefly, the rest of my comments will follow;You say:
Actually, the mechanism repairs C-->T deamination errors.I say:
That is correct. C-->T tranversion will be repaired. However, it is important to realize that cytosince methylation can affect mutations through other mechanisms. These occur because 5-methyl cytosine is itself mutagenic. It can undergo spontaneous hydrolytic deamination to cause C-->T tranversions. This enhanced mutagenesis is seen in the germ line of all organisms that methylate their DNA. Furthermore, approximately 50% of inactivating pointmutations in the coding region of p53 in somatic cells occur at methylated cytosines (Science, 249:1288-90). That is half of the mutations! This mechanism will assuredly contribute to the illusion of common descent.If you’ll check, I think you’ll find that 5-methylcytosine is implicated in G-->T mispairing. The glycosylases TDG or MBD4 are the specifics for repair of this particular error. You seem to be confusing repair mechanisms such as the glycosylases with the mutagens that cause the problem in the first place. On another note, here’s a good article on the repair of 8-oxo-G errors: Substrate specificity and Reaction Mechanisms of Murine 8-Oxoguanine-DNA glycosylase.Please provide the full reference for the article you cite.I say:
It was you who refered to this article last week. I read it and observed that it describes a non-random mechanism of mutations.You say:
If you're going to use something as evidence, we need to be able to check it.You are right. However, I thought you would recognise your own reference. Next time I will not be so sloppy.Best wishes,
peter

Hi PeterDear mammuthus,I think that you are a bit confused now. It was Quetzal's question. But anyway, Quetzal will be happy (?) I guess.M:If I am not mistaken I pointed out that I mis-credited Quetzals question to you and posted my error and an apology to both you and Quetzal.PB:
However, I am aware of these studies and the authors conclude that "three lines of evidence suggest that they [genomic changes] are mostly due to IS-transposition and other types of chromosomal rearrangements. First, [..], point mutations are NOT [caps are mine, PB] abundant in these evolving populations. Second, the extent of genomic change [..] was similar among lines that had become genetic mutators and those that had wild-type point-mutation rates. [..] Finally, we observed significant changes in the copynumber of certain IS-elements [..], most easily explained by transposition and deletion events that produce gains and losses of copies, respectively" (Papdopoulos et al, PNAS 1999, 96:3807)MY RESPONSE:
Thus, although populations change over time, this is not due to the change of nucleotides and therefore not due to changing DNA sequences. The only changes are the ORDER of the sequences, the order of transposable elements and therefore --in my opinion-- gene expression is altered. That is all what is required for distinct phenotypes. No information added or gained. All information was already present. It has been shuffled due to exision and reintegration of DNA through specific proteins (endonucleases, integrases, ligases etcetera). The only thing that was added to the genome in certain cases were additional copies of transposable elements. All this after 10.000 generations! This is NO evolution, it is VARIATION INDUCTION generated by a genetic mechanism already present in the original cells. Similar observations have been done in Enterococcus (Nature 2002, 13 june), that is able to actively shuffle genes on a DNA island in response to antibiotics. Apparently, bacteria have a very plastic genome.
It perfectly fits in the multipurpose genome hypothesis.M: Actually Peter, it does not. When a retrotranposon transposes it leaves the original copy behind and inserts new ones in other parts of the genome. Thus, it is novel variation. In addition, novel infections lead to new classes of retrotransposons that can then infect, integrate, and diverge i.e. HERV-W family present in Old World monkey but absent from New World Monkeys and strepsirhines.You are also presenting a logical fallacy in saying that the change does not count because the source of the mutation i.e. transposon was already present. That is like saying that all mutations are not novel because there is DNA in the cell or a C-T is not novel because there are other C's and T's. New content comes in via horizontal transfer, infection, etc. and then is mutated or shuffled. This is the mutation resources that drive evolution.I will ask again if you are going to respond to my other points I brought up? I would like to believe that you are contemplating responses or just missed them. If so I look forward to your response and continued debate.best wishes,
M

PB:
That is correct. C-->T tranversion will be repaired. However, it is important to realize that cytosince methylation can affect mutations through other mechanisms. These occur because 5-methyl cytosine is itself mutagenic. It can undergo spontaneous hydrolytic deamination to cause C-->T tranversions. This enhanced mutagenesis is seen in the germ line of all organisms that methylate their DNA. Furthermore, approximately 50% of inactivating pointmutations in the coding region of p53 in somatic cells occur at methylated cytosines (Science, 249:1288-90). That is half of the mutations! This mechanism will assuredly contribute to the illusion of common descent.M: However, which C-T occurs is still a random process. And when one compares the tranversion rate it is also not insignificantly small. None of this can logically "assuredly contribute to the illusion of common descent."Again, if you find that your mtDNA sequence is identical to your mothers is this assuredly an illusion of parentage? This is of necessity if your hypothesis is correct....and think of the benefits..no more having to remember to send mothers day (or fathers day) cards .)

Gee - why isn't Peter B. blowing off my citation on the accuracy of molecular phylogenetics?I'm sad...

My guess is that if morphometrics and software testing metrics can ever be weded to COLLEGETOWN USA the Where of this will only be found in the report, but Percy is still navigating the fishy waters fairly well...

dear mammuthus,You say:I will ask again if you are going to respond to my other points I brought up? I would like to believe that you are contemplating responses or just missed them. If so I look forward to your response and continued debate.I say:I forgot about them but I will certainly respond to them next week.best wishes,
Peter

quote:

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Originally posted by peter borger:
dear mammuthus,

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You say:

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I will ask again if you are going to respond to my other points I brought up? I would like to believe that you are contemplating responses or just missed them. If so I look forward to your response and continued debate.

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I say:

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I forgot about them but I will certainly respond to them next week.

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best wishes,
Peter

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***********************Hi Peter,
Looking forward to it. I basically put down a bunch of things that came to mind a few posts ago regarding your hypothesis and would like to debate them with you.cheers,
M

Dear Mammuthus,You write:quote:
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Originally posted by peter borger:
dear mammuthus,
You say:I will ask again if you are going to respond to my other points I brought up? I would like to believe that you are contemplating responses or just missed them. If so I look forward to your response and continued debate.I say:I forgot about them but I will certainly respond to them next week.best wishes,
Peter--------------------------------------------------------------------------------***********************Hi Peter,
Looking forward to it. I basically put down a bunch of things that came to mind a few posts ago regarding your hypothesis and would like to debate them with you.I say:Could you please indicate the mailnumber'and/or specific issues I have to address. Than I will prepare properly and elaborate nonrandomness and multipurpose in more detail. Thanks in advance,Best wishes,
Peter

Hi Peter,
Post 42 to 45 in this thread for example went unanswered.
Unfortunately, others are buried in other threads but at least I could easily find the ones in this thread. I think the rest are in the "Endosymbiotic thoery is wrong thread"cheers,
M

found some more...posts 30, 36, 37 (Quetzals post) and 40 in the Endosymbiotic theory is wrong thread...

Thread closed at request of originator Peter Borger.--------------------EvC Forum Administrator

Hi peter...this really belongs on the other NRM thraed, but it is closed. I have tried to read through the threads and it is possible I have missed the answer to this question, so apaolgies if I have.Why cannot the similarities in the IG5 gene within geographically separate populations of drosophilia melanogaster not be due to gene flow in view of the fact they are really the same species?This may be a dumb question as I am out of my depth on this forum.Also can you explain the NRM between the so called "sibling species"Thanks[This message has been edited by judge, 01-15-2003][This message has been edited by judge, 01-15-2003]

quote:

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Originally posted by Percipient:
The word random doesn't even appear in the article. The sentence you quoted only notes that, as was already well known, some parts of the genome are more susceptible to mutation than others, and the increased levels of radiation have a greater impact on these "hotspots". Where the mutation takes place is random, but the probability of where the mutation might occur is not equal everywhere.

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An analogy would be buildings in an earthquake. Which buildings fall is random, but weaker buildings are more likely. Correspondingly, some portions of the genome are more resistant to change than others.

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--Percy

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As is usually the case, buildings are designed by an intelligent designer, including being specifically designed to withstand earthquakes. Great analogy to show that Intelligence is required, NOT random mutation or natural selection.Regards,
S------------------
"You can no more alter God than a pebble can alter the rhythm of the Pacific."

Uh, Sonnikke, the anology was about knocking down the buildings, not designing and constructing them. It took you since October to think this up?--Percy