quote:
Originally posted by John Paul:
John Paul:
Um, I read the article you cited- I found it here:
That should take care of that silly accusation.
Given that you can't respond substantively I'm not sure what linking to it proves. However, from you later comments it is clear you didn't read it.
[QUOTE]
As for the article I linked to, this snippet is relevant:
"So I think there is a mechanistic process that has produced many of the Pseudogenes that we have, rather than a random process. If the Pseudogene is truly defective and if the mutations are truly found in patterns (not random), then the idea that it's a common mechanism is possible. Viruses have enzymes that, under the same conditions, do repeatable reactions.
If the DNA in Humans, Chimps, Monkeys, etc., are very similar, then if they are all infected by the same virus, would we expect the virus to do the same thing in the different species? I think so.
The "dreaded endogenous retroviral sequence common to both chimp and human DNA" is probably the major example of Common Mechanism. Viral enzymes (proteins) react with specific DNA sequences. If both chimp and human DNA have the same active sites, I would expect the viral proteins to react in the same exact way to both human and chimp.
Common descent or common Ancestor is not the only answer."
That should take care of silly accusation 2.
Like I said before- this hypothesis can be tested in a lab by taking 2 different (but similar) species and infecting them with the same virus. The evolutionary hypothesis has no such test.
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But your test has been disproven and the evidence of this is cited in the article you supposedly read:
22. Varmus, H. E. & Swanstrom, R. (1984) in RNA Tumor Viruses, eds. Weiss, R., Teich, N. M., Varmus, H. E. & Coffin, J. M. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 369-512.
23. Brown, P. O. (1997) in Retroviruses, eds. Coffin, J. M., Hughes, S. H. & Varmus, H. E. (Cold Spring Harbor Laboratory Press, Plainview, NY).
24. Withers-Ward, E. S., Kitamura, Y., Barnes, J. P. & Coffin, J. M. (1994) Genes Dev. 8, 1473-1487 [Abstract].
quote:
Endogenous retrovirus loci provide no less than three sources of phylogenetic signal, which can be used in complementary fashion to obtain much more information than simple distance estimates of homologous sequences. First, the distribution of provirus-containing loci among taxa dates the insertion. Given the size of vertebrate genomes (>1 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14). Furthermore, integrated proviruses are extremely stable: there is no mechanism for removing proviruses precisely from the genome, without leaving behind a solo LTR or deleting chromosomal DNA. The distribution of an ERV among related species also reflects the age of the provirus: older loci are found among widely divergent species, whereas younger proviruses are limited to more closely related species. In theory, the species distribution of a set of known integration sites can be used to construct phylogenetic trees in a manner similar to restriction fragment length polymorphism (RFLP) analysis.
So you read it, huh? Not very well apparently. Retroviral insertions do occur within the genome randomly. Thus, the argument you makes fail. Additionally, retroviral insertions occur in a pattern that is nested hierarchy that fits evolutionary predictions.
Would you care to explain that too?
Of course, to add problems to your claim, the different lineages match based upon their expected rates of insertions with the expected timeline of evolution. All just coincidence?
http://www3.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=94285820&form=6&db=m&Dopt=r
It is bad enough to not to read, but lying about reading is just bad form.
Cheers,
Larry