Well, if you're trying to prove a claim of universal common ancestry then this evidence is insufficient because there are no examples of ‘shared errors’ that link mammals to other branches of the genealogic tree.This example is of course only for the species in the diagram. I don't follow the research on retroviruses closely enough to tell what parts of the evolutionary tree has been tied together like this. Of course, I'm not trying to prove anything, as that's really outside of science's scope (unless you're of the school that includes math in the scientific realm), but merely to present evidence.
It also is insufficient to establish common ancestry because it is based on the the presumption that the retroviruses are non-functionalOf course this evidence can be falsified, just like DNA tests to establish paternity could, but that has yet to happen.
Also there is some evidence to support the idea that some of these may serve functions, and that their insertion is not entirely random.Such as?
600
How? If the same phenomena occured in two species that are not believed to have shared a recent common ancestor then it could just as easily be chalked up to homoplasy. Common ancestry accommodates either phenomena but it certainly does not predict them and therefore cannot be falsified by their absence or confirmed by their presence. There is nothing wrong with a theory that can accomodate widely different results, but one can't turn around then and claim that one of those results is evidence for the theory.
Cordially,
It also is insufficient to establish common ancestry because it is based on the the presumption that the retroviruses are non-functionalOf course this evidence can be falsified, just like DNA tests to establish paternity could, but that has yet to happen.
Also there is some evidence to support the idea that some of these may serve functions, and that their insertion is not entirely random.Such as?
"There were identified ‘hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically."
"...sometimes the hosts exploit the capacity of TEs to generate variations for their own benefit. The retroelements can come out as traveling donors of sequence motifs for nucleosome positioning, DNA methylation, transcriptional enhancers, poly(A) addition sequences, splice sites, and even amino acid codons for incorporation into open reading frames of encoded proteins [8, 9].The number of described cases in which retroelement sequences confer useful traits to the host is growing [11, 12, 13]. Retropositions can therefore be considered as a major pacemaker of the evolution that continues to change our genomes [14, 15, 16]. In particular, HERV elements could interact with human genome through (i) expression of retroviral genes, (ii) human genome loci rearrangement following the retroposition of the HERVs or (iii) the capacity of LTRs to regulate nearby genes [2, 3, 4, 5]. A plethora of solitary LTRs comprises a variety of transcription regulatory elements, such as promoters, enhancers, hormone-responsive elements, and polyadenylation signals. Therefore the LTRs are potentially able to cause significant changes in expression patterns of neighboring genes."
Cordially,