作者: Felipe Karam Teixeira , Martyna Okuniewska , Colin D. Malone , Rémi-Xavier Coux , Donald C. Rio
DOI: 10.1038/NATURE25018
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摘要: Transposable elements can drive genome evolution, but their enhanced activity is detrimental to the host and therefore must be tightly regulated. The Piwi-interacting small RNA (piRNA) pathway vital for regulation of transposable elements, by inducing transcriptional silencing or post-transcriptional decay mRNAs. Here we show that piRNAs piRNA biogenesis components regulate precursor mRNA splicing P-transposable element transcripts in vivo, leading production non-transposase-encoding mature isoform Drosophila germ cells. Unexpectedly, do not act reduce transcript levels P-element transposon during P-M hybrid dysgenesis, a syndrome affects germline development Drosophila. Instead, mechanistically achieved together with piRNA-mediated changes repressive chromatin states, relies on function Piwi-piRNA complex proteins Asterix (also known as Gtsf1) Panoramix (Silencio), well Heterochromatin protein 1a (HP1a; encoded Su(var)205). Furthermore, this machinery, Flamenco cluster, only controls accumulation Gypsy retrotransposon also regulates mRNAs cultured ovarian somatic cells, process required infectious particles lead heritable transposition events. Our findings identify new role essential Piwi protecting against mobility, provide model system studying structure modulating alternative development.