Is there a role for endogenous retroviruses to mediate long-term adaptive phenotypic response upon environmental inputs?
Author(s) -
Jafar Sharif,
Yoichi Shinkai,
Haruhiko Koseki
Publication year - 2012
Publication title -
philosophical transactions of the royal society b biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.753
H-Index - 272
eISSN - 1471-2970
pISSN - 0962-8436
DOI - 10.1098/rstb.2011.0340
Subject(s) - biology , epigenetics , endogenous retrovirus , gene , genetics , genome , histone , dna methylation , phenotype , retrotransposon , placentation , long terminal repeat , transposable element , computational biology , gene expression , pregnancy , fetus , placenta
Endogenous retroviruses (ERVs) are long terminal repeat-containing virus-like elements that have colonized approximately 10 per cent of the present day mammalian genomes. The intracisternal A particles (IAPs) are a class of ERVs that is currently highly active in the rodents. IAP elements can influence the transcription profile of nearby genes by providing functional promoter elements and modulating local epigenetic landscape through changes in DNA methylation and histone (H3K9) modifications. Despite the potential role for IAPs in gene regulation, the precise genomic locations where these elements are integrated are not well understood. To address this issue, we have identified more than 400 novel IAP insertion sites within/near annotated genes by searching the murine genome, which suggests that the impact of IAP elements on local and/or global gene regulation could be more profound than was previously expected. On the basis of our independent analyses and already published reports, here we argue that IAPs and ERV elements in general could have an evolutionary role for modulating phenotypic plasticity upon environmental inputs, and that this could be mediated through specific stages of embryonic development such as placentation during which the epigenetic constraints on IAP elements are partially relaxed.
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