Abstract
We detected 19 complete endogenous retroviruses of the K family in the genome of rhesus monkey (Macaca mulatta; RhERV-K) and 12 full length elements in the genome of the common chimpanzee (Pan troglodytes; CERV-K). These sequences were compared with 55 human HERV-K and 20 CERV-K reported previously, producing a total data set of 106 full-length ERV-K genomes. Overall, 61% of the human elements compared to 21% of the chimpanzee and 47% of rhesus elements had estimated integration times less than 4.5 million years before present (MYBP), with an average integration times of 7.8 MYBP, 13.4 MYBP and 10.3 MYBP for HERV-K, CERV-K and RhERV-K, respectively. By excluding those ERV-K sequences generated by chromosomal duplication, we used 63 of the 106 elements to compare the population dynamics of ERV-K among species. This analysis indicated that both HERV-K and RhERV-K had similar demographic histories, including markedly smaller effective population sizes, compared to CERV-K. We propose that these differing ERV-K dynamics reflect underlying differences in the evolutionary ecology of the host species, such that host ecology and demography represent important determinants of ERV-K dynamics.
Highlights
A considerable proportion (,45%) of the primate genome consists of copies of mobile genetic elements [1]
We described several new complete endogenous retroviruses (ERVs)-K elements in the genomes of the common chimpanzee (Pan troglodytes) and rhesus monkey (Macaca mulatta) and compared them to those found in humans
For the first time, that the demographic history of the host may be a major factor determining the dynamics of an endogenous retrovirus
Summary
A considerable proportion (,45%) of the primate genome consists of copies of mobile genetic elements [1]. These elements are divided into two classes based on their mechanism of mobilization: those involving an RNA intermediate, or those that transpose via DNA excision and reintegration into the host genome (transposons). ERVs are relics of ancient viral infection events in the germ line, followed by long-term vertical transmission. They can increase in copy number by means of active replication (in cis or in trans) or by chromosomal duplication [2], and represent about 3% of all transposable elements (TE) related sequences. Because the LTRs (long terminal repeats) of proviruses carry transcriptional regulatory elements, such as promoters and enhancers, its likely that the insertion of a provirus, or only its LTRs, near genes or regulatory regions will be detrimental to host fitness [3,4,5]
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