The nuclear exosome is required for Piwi-piRNA mediated co-transcriptional gene silencing [ChIP-seq]
Co-transcriptional gene silencing mediated by small RNA pathways is primarily studied in the context  of heterochromatin formation. These pathways are known to target nascent RNAs, yet their intersection  with cellular processes determining the fate of the nascent transcripts remain unclear. We report that the  nuclear exosome, the central cellular 3' to 5' exo-ribonuclease complex, is required for transposon  repression through the Piwi-piRNA pathway in Drosophila. Using somatic ovarian cells, where piRNA  biogenesis and piRNA-guided silencing are separated, we demonstrate that the three adaptor complexes  of the nuclear exosome –PAXT, NEXT, and TRAMP– are redundantly required for degrading piRNA  target transcripts. Furthermore, we identify two paralogous proteins, Creator-1 and Creator-2, as piRNA  pathway factors that physically connect the exosome to the Piwi-silencing complex through a novel  poly-proline binding domain. Our findings uncover an evolutionarily conserved principle whereby the  nuclear RNA exosome is integral to diverse co-transcriptional silencing processes controlled by  small RNAs. Overall design: Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modification H3K9me3 in OSC reporter cells. And ChIP-seq for histone modification H3K9me3 in OSCs after siRNA mediated depletion of Piwi, CG31510&CG7065, Dis3, Rrp40, Rrp41, dZfc3h1&dZcchc8, or Mtr4, compring to control knockdown.