Meiotic synapsis and recombination ensure correct homologous segregation and genetic diversity. Asynapsed homologs are transcriptionally inactivated by meiotic silencing, which serves a surveillance function and in males drives meiotic sex chromosome inactivation. Silencing depends on the DNA damage response (DDR) network, but how DDR proteins engage repressive chromatin marks is unknown. We identify the histone H3-lysine-9 methyltransferase SETDB1 as the bridge linking the DDR to silencing in male mice. At the onset of silencing, X chromosome H3K9 trimethylation (H3K9me3) enrichment is downstream of DDR factors. Without Setdb1, the X chromosome accrues DDR proteins but not H3K9me3. Consequently, sex chromosome remodeling and silencing fail, causing germ cell apoptosis. Our data implicate TRIM28 in linking the DDR to SETDB1 and uncover additional factors with putative meiotic XY-silencing functions. Furthermore, we show that SETDB1 imposes timely expression of meiotic and post-meiotic genes. Setdb1 thus unites the DDR network, asynapsis, and meiotic chromosome silencing.
Pubmed ID: 30393076 RIS Download
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View all literature mentionsThis monoclonal targets Cleaved PARP antibody [E51]
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View all literature mentionsThis polyclonal targets USP7
View all literature mentionsThis monoclonal targets ubiquityl-Histone H2A clone E6C5
View all literature mentionsThis polyclonal targets SHEEP ANTI HUMAN MDC1 (aa1883-2089)
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View all literature mentionsThis monoclonal targets KAP1
View all literature mentionsThis polyclonal targets RAD51
View all literature mentionsThis monoclonal targets α-Tubulin
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