GSE123741
ChIPseq on H3K27me3 and H2AK119Ub on Xist-tetOP ?B+C cell line, after 2 days of differentiation, with or without DOX induction
Xist RNA has been established as the master regulator of X-chromosome inactivation in female eutherian mammals but its mechanism of action remain unclear. By creating novel Xist mutants at the endogenous locus in mouse embryonic stem cells, we dissect the role of most of the conserved A-F repeats. We find that transcriptional silencing can be uncoupled from Polycomb repressive complex 1 and 2 (PRC1/2) recruitment, which requires repeats B and C. Xist ?B+C specifically looses interaction with PCGF3/5 subunits of PRC1, while binding of other Xist partners are largely unaffected. However, a slight relaxation of transcriptional silencing in Xist ?B+C indicates a role for PRC1/2 proteins in early stabilization of gene repression. Distinct structural modules within the Xist RNA are therefore involved in the convergence of independent chromatin modification and gene repression pathways, with Polycomb recruitment only being of moderate relevance in the initiation of silencing. Overall design: Native ChIPseq on H3K27me3 and H2AK119Ub on  Xist-tetOP ?B+C cell line, after 2 days of differentiation, with or without DOX induction, in replicates.