SRA

Polycomb repressor complexes (PRCs) are important chromatin modifiers fundamentally implicated in pluripotency and cancer. Polycomb silencing in embryonic stem cells (ESCs) can be accompanied by active chromatin and primed RNA polymerase II (RNAPII), but the relationship between PRCs and RNAPII remains unclear at the genome-wide level. We mapped PRC repression markers and four RNAPII states in ESCs using ChIP-seq, and found that PRC-targets exhibit a range of RNAPII variants. Firstly, developmental PRC-targets are bound by unproductive RNAPII (S5p+S7p- S2p-) genome-wide. Sequential ChIP, Ring1B-depletion and genome-wide correlations show that PRCs and RNAPII-S5p physically bind to the same chromatin and functionally synergize. Secondly, we identify a cohort of genes marked by PRC and elongating RNAPII (S5p+S7p+S2p+); they produce mRNA and protein, and their expression increases upon PRC1 knockdown. We show that this novel group of PRC-targets switch between active and PRC-repressed states within the ESC population, and that many have roles in metabolism. **Correction (Mar 14, 2012): Due to curation error, runs for SRX112177 and SRX112179 switched, specifically, Run SRR391034.1 was removed from experiment SRX112177 (GSM850468) and added to experiment SRX112179 (GSM850470) as SRR391034.3 Run SRR391040.1 was removed from experiment SRX112179 (GSM850470) and added to experiment SRX112177 (GSM850468) as SRR391040.3 Overall design: Examination of 4 different RNAPII modifications (S5p, S7p, 8WG16, S2p), and the histone modifications H2Aub1 and H3K36me3 in mouse ES cells