Adaptive genome defense mechanisms in the ovarian somatic cell niche silences ancient infectious retroelements
Abstract
Transposable elements (TEs) are kept silent in the germline of most animals by the
PIWI interacting RNA (piRNA) pathway. The piRNA pathway is a form of adaptive
immunity and has been proposed to be in an 'evolutionary arms race' with the TE
elements that they silence. The best example of this, are Ty3/gypsy
retrotransposons in Drosophila melanogaster, that acquired env proteins, called
errantiviruses. These errantiviruses are expressed in the ovarian somatic cell niche
and utilize their membrane fusion proteins to enter the adjacent germline cells, thus
avoiding the highly conserved germline piRNA pathway. As an adaptation to this,
Drosophila melanogaster have duplicated piRNA biogenesis factors, and have
started to express piRNAs targeting these elements in the somatic cell niche as well.
This thesis will establish three main points. Firstly, rapid divergence of piRNA
biogenesis, and loss of piRNA biogenesis factors, does not impact efficient
transposon silencing in Drosophila. Secondly, errantiviruses and env containing
retrotransposons are ubiquitous, and actively transposing in almost every metazoan
branch. Finally, somatic transposon defence mechanisms are highly conserved to
silence errantiviruses, and they have likely existed in the same cell niche over long
periods of time.
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