Abstract
The PIWI-interacting RNA (piRNA) pathway is a small RNA-based immune system that controls the expression of transposons and maintains genome integrity in animal gonads. In Drosophila, piRNA-guided silencing is achieved, in part, via co-transcriptional repression of transposons by Piwi. This depends on Panoramix (Panx); however, precisely how an RNA binding event silences transcription remains to be determined. Here we show that Nuclear Export Factor 2 (Nxf2) and its co-factor, Nxt1, form a complex with Panx and are required for co-transcriptional silencing of transposons in somatic and germline cells of the ovary. Tethering of Nxf2 or Nxt1 to RNA results in silencing of target loci and the concomitant accumulation of repressive chromatin marks. Nxf2 and Panx proteins are mutually required for proper localization and stability. We mapped the protein domains crucial for the Nxf2/Panx complex formation and show that the amino-terminal portion of Panx is sufficient to induce transcriptional silencing.
Highlights
The PIWI-interacting RNA (piRNA) pathway is a small RNA-based immune system that represses transposable elements in animal gonadal tissues (Czech et al, 2018)
We find that the amino-terminus of Panx delivers the critical silencing signal, as it is necessary and sufficient to trigger the deposition of repressive chromatin marks if tethered to a reporter construct, while its carboxyl-terminal region is involved in the interaction with Nuclear Export Factor 2 (Nxf2)
Nxf2 is a homolog of the general messenger RNA export factor Nxf1 but was reported previously as being dispensable for canonical mRNA transport in Schneider 2 (S2) cells (Herold et al, 2001; Herold et al, 2003)
Summary
The piRNA pathway is a small RNA-based immune system that represses transposable elements in animal gonadal tissues (Czech et al, 2018). In contrast, operates in the nucleus where it instructs the co-transcriptional gene silencing (TGS) of transposon insertions (Brennecke et al, 2007; Klenov et al, 2011; Sienski et al, 2012). Target silencing is achieved via recruitment of histone modifying enzymes that deposit repressive chromatin marks, mainly trimethylation of Lysine 9 on Histone 3 (H3K9me3) (Iwasaki et al, 2016; Klenov et al, 2014; Le Thomas et al, 2013; Rozhkov et al, 2013; Sienski et al, 2012; Wang and Elgin, 2011). How Panx recruits these histone modifying enzymes and what other factors participate in this process remains an outstanding question
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