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

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

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

Dear Judge,Judge: 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.PB: Geographically seperated populations says it all. Gene flow could be explanatory under the assumption that the populations have been infiltrated by migrating individuals from italy, peru and USA. However, the other mutations refute this possibility.Judge: Also can you explain the NRM between the so called "sibling species"PB: could you please point out the exact positions.Best wishes,
Peter

Dear Admin,You are right. The thread should have been closed. Please close it(To be continued in other threads that will further degrade evolutionism)Best wishes,
Peter