Epigenetic targeting of transposon relics: beating the dead horses of the genome?

Transposable elements (TEs) have been seen as selfish genetic elements that can propagate in a host genome. Their propagation success is however hindered by a combination of mechanisms such as mutations, selection, and their epigenetic silencing by the host genome. As a result, most copies of TEs in a given genome are dead relics: their sequence is too degenerated to allow any transposition. Nevertheless, these TE relics often, but not always, remain epigenetically silenced, and if not to prevent transposition anymore, one can wonder the reason for this phenomenon. The mere self-perpetuating loop inherent to epigenetic silencing could alone explain that even when inactive, TE copies remain silenced. Beyond this process, nevertheless, antagonistic selective forces are likely to act on TE relic silencing. Especially, without the benefit of preventing transposition, TE relic silencing may prove deleterious to the host fitness, suggesting that the maintenance of TE relic silencing is the result of a fine, and perhaps case-by-case, evolutionary trade-off between beneficial and deleterious effects. Ultimately, the release of TE relics silencing may provide a 'safe' ground for adaptive epimutations to arise. In this review, we provide an overview of these questions in both plants and animals.

Automated summary

Transposable elements (TEs) are selfish genetic elements that can propagate in a host genome. While most TE copies are degenerated and unable to transpose, they often remain silenced through epigenetic mechanisms. The maintenance of TE relic silencing may be a trade-off between beneficial and deleterious effects, as it may prove detrimental to the host fitness without the benefit of preventing transposition. However, the release of TE relic silencing may provide opportunities for adaptive epimutations to occur.