Genetic evidence of primate evolution

Since genetic evidence is JP's standard, I thought I'd add an abstract to another article in the Aug 31, 1999 Proceedings of the National Academy of Science. Perhaps JP would like to get the article and discuss it in detail?Constructing primate phylogenies from ancient retrovirus sequences
Welkin E. Johnson and John M. Coffin
The genomes of modern humans are riddled with thousands of endogenous retroviruses (HERVs), the proviral remnants of ancient viral infections of the primate lineage. Most HERVs are nonfunctional, selectively neutral loci. This fact, coupled with their sheer abundance in primate genomes, makes HERVs ideal for exploitation as phylogenetic markers. Endogenous retroviruses (ERVs) provide phylogenetic information in two ways: (i) by comparison of integration site polymorphism and (ii) by orthologous comparison of evolving, proviral, nucleotide sequence. In this study, trees are constructed with the noncoding long terminal repeats (LTRs) of several ERV loci. Because the two LTRs of an ERV are identical at the time of integration but evolve independently, each ERV locus can provide two estimates of species phylogeny based on molecular evolution of the same ancestral sequence. Moreover, tree topology is highly sensitive to conversion events, allowing for easy detection of sequences involved in recombination as well as correction for such events. Although other animal species are rich in ERV sequences, the specific use of HERVs in this study allows comparison of trees to a well established phylogenetic standard, that of the Old World primates. HERVs, and by extension the ERVs of other species, constitute a unique and plentiful resource for studying the evolutionary history of the Retroviridae and their animal hosts.Since I have university access I've already downloaded the paper. When do you think you can get a copy and comment JP?Cheers,
Larry

Just so you know, science is designed to test hypotheses and thus provide an answer to questions. It isn't a post modern exercise in whining as you have attempted to portray it. Now, either you address the specific evidence or stop your whining about bias. A hypothesis is a test and it is dependent on objective evidence. Whining that such a test produces a bias is one of the most inane arguments available given a test should result in a bias towards the correct answer.Cheers,
Larry

I have a suggestion. Why don't you read the articles cited to you? You have not bothered to read either the whale article or this one. How do you make assertions about them if you don't read?I expect you to either respond in detail to the articles, or admit you have no response. You "article" simply asserts that such things are consistent with creationism without ever explaining how such non-functional evidence would occur in identical locations in the genome in different populations over a 6000 year history which is necessary given they are caused by retroviruses. Provide how creationism accounts for this.A retrovirus wouldn't be placed in the same portion for any rational reason. The assertion is ludicrous and baseless.. Or can you provide a specific example of how this would happen--not a similar mechanism as is so often cited, but NEVER identified.Just curious,
Larry

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[This message has been edited by lbhandli, 02-04-2002]

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Originally posted by John Paul:
John Paul:
Um, I read the article you cited- I found it here:

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That should take care of that silly accusation.

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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.

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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.

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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.

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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.[/B][/QUOTE]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].

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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.

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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=rIt is bad enough to not to read, but lying about reading is just bad form.Cheers,
Larry

I'd like for some creationists to respond to where this thread stopped since John Paul has left us.