Continuing the critique of Liu.[quote]

  • Contributions of endogenous retroviruses to the host: syncytins

  • Retroelements including ERVs are normally suppressed from expression or transposition by extensive DNA methylation, RNA interference, heterochromatin formation, etc., to maintain genomic stability of the cell. Failure of the cell to control ERVs can lead to mutations or diseases.8,10,11 As a matter of fact, improper activation of endogenous retroviruses has been associated with many human cancers and autoimmune disorders.11 Complex interplay between retroelements and gene silencing mechanisms suggests ERVs are integral parts of the genome.[/quote]

So because so many ERVs are still able to create havoc in our cells unless they are 'controlled', that makes them integral parts of the genome!

  • [quote]
  • However, some of these genetic elements are expressed at certain stages of the host’s lifetime to the benefit of the host. Several instances of beneficial ERVs have been noticed. (1) Regulation, mainly activation, of neighboring (downstream) genes during embryonic development of the mouse.12 (2) Regulation of human genes expressed in the placenta (e.g. pleiotropin) and somatic tissues (e.g. apolipoprotein C1 in the liver and β-amylase in the salivary gland).8,13 (3) Immunomodulation, including induction of immunotolerance to self antigens and immunization against exogenous retroviruses.8,13 (4) The envprotein of HERV-W and HERV-FRD serving as fusogenic factors (syncytins) during human trophoblast development.14,15 (5) Other roles such as mammalian tissue organization.16 Many of these genes are expressed during genome-wide DNA demethylation in gametogenesis (formation of eggs or sperm) and embryonic development, therefore are important for reproduction.[/quote]


Basically, Liu is trying to imply that because certain parts of certain ERVs perform an essential function, then at least some ERVs are there by design. 1) Whether they are there by design or not, the best explanation of common ERVs among creatures is common ancestry. This applies to creatures with corresponding ERVs whether or not they are the same kinds of creature. 2) Very few ERVs have parts that perform any beneficial function. What about the other parts that do not? What about all the other ERVs? Why are they there? 3) What is the problem with the notion that components of ERVs can be co-opted by evolutionary processes? It is far more likely that a ready-made approximation to a useful gene gets co-opted than a useful gene arising from complete junk. And a failure to comprehend how ancestors could get by without what is now an essential gene is just that - a failure of comprehension. This study investigates the evolution of syncytin 1 in apes and monkeys. The following diagram taken from the paper maps out just how the HERVW env gene evolved into syncytin 1. Old world monkeys reproduce just fine - indeed with enthusiasm - without a functional syncytin derived from the HERVW env gene.

[noparse]
http://jhered.oxfordjournals.org/content/97/2/100/F2.expansion.html
[/noparse]

  • Evolutionary analysis of Syncytin 1 in hominoids and Old World monkeys. Neighbor-joining tree based on 2,331 bp of Syncytin 1 sequence in 14 primate species, with the bootstrap values of 1,000 replicates indicated in boldface for all the nodes. Gene-inactivating mutations and their corresponding position with respect to the human coding sequence are shown below the branches: asterisks, stop codons; black upward triangles, frameshift insertions; black downward triangles, frameshift deletions. Deletions that do not affect the reading frame are represented as empty downward triangles. Ka/Ksratios according to the PAML free-ratio model are shown in italics above each branch. Dashes indicate branches with Ks = 0. Branch length in the tree corresponds to the number of nucleotide substitutions per codon. In these analyses, the HERV-W family consensus sequence, HERV17 (Jurka 2000), was used as the outgroup, but very similar results were obtained when six sequences representing ancestral HERV-W insertions in the catarrhine lineage derived from the full-length env copies in the human, chimpanzee, and rhesus genome were used. The most parsimonious scenario for the generation of a stop codon in the catarrhine lineage from the original TGC sequence and its reversion in hominoids is represented inside rectangles.

And from Evidence for the Evolutionary Model, [noparse]
http://www.evolutionarymodel.com/ervs.htm
[/noparse]
  • There is no question that some ERVs have functions in organisms, but there are no wholly functional ERVs—only functional components, with the remainder deleted or mutated into non-functionality.

  • For instance, the contribution of enJS56A1 and enJS5F16 (of the mere ~20 enJSRVs) to placental growth/differentiation regulation is achieved solely by their env genes with open reading frames (Dunlap et al., 2006; Palmarini et al., 2000). Although they also have an open gag reading frame (causing gag-gag interaction that restricts pathogenic JSRVs), they are the only ones known to have this (Mura et al., 2004). And every studied enJSRV has a closed pol reading frame (Murcia, Arnaud, & Palmarini, 2007).

  • Another example is the transcriptional contribution of LTRs to genes' promoters:

  • 1) Not only are most ERVs not at a loci that even makes it possible for them to contribute to transcriptional activity, but most ERVs have recombined into solo LTRs. Since only the LTRs of active full-length ERVs can contribute (Cohen, Lock, & Mager, 2009, p.107), even most ERVs in the right position have no effect. Just as with enJSRVs, these ERVs represent a very small percentage of the whole.

  • 2) The actual genes of these ERVs contribute nothing—only their promoter sequence-rich LTRs do. Again, just as with enJSRVs, these are examples of functional ERV components, rather than functional ERVs.

  • It is the same with every case observed; again, there are no "functional ERVs;" only a small percentage of ERVs with functional components.

  • But it's a moot point, because we know that ERVs are insertions:

  • The hallmark of an insertion is a displacement of chromosomal DNA, and the hallmark of insertion by integrase is the presents of target site duplication, due to the way it attacks the 5' and 3' phosphodiester bonds with an offset of a few base pairs (Skinner et al., 2001). Since ERVs are accompanied by target site duplications and DNA displacement, they are necessarily endogenized/fixed proviral insertions.

  • So any functional components are necessarily post-insertion exaptations, and the fact that they are necessarily insertion means that they can not be part of any 'original design.' The issue of functionality is simply a red herring, when discussing how ERVs necessitate common ancestry.

  • For an understanding of scaffolding (p.365-366) and exaptation (p.361-363), including various "paths to exaptation," refer to the first half (p.358-366) of "The Evolution of Complex Organs" by Dr. Gregory (2008).