Polycomb repressor complexes (PRCs) are vital chromatin modifiers Caspase fundamentally implicated in pluripotency and cancer. Polycomb silencing in embryonic stem cells (ESCs) is usually accompanied by energetic chromatin and primed RNA polymerase II (RNAPII), but the connection among PRCs and RNAPII remains unclear genome-wide. We mapped PRC repression markers and four RNAPII states in ESCs utilizing ChIP-seq, and found that PRC targets exhibit a variety of RNAPII variants. Initially, developmental PAC targets are bound by unproductive RNAPII (S5p(+)S7p(-)S2p(-)) genonne-wide. Sequential ChIP, Ring1B depletion,phosphatase inhibitor and genome-wide correlations show that PRCs and RNAPII-S5p physically bind to the exact same chromatin and functionally synergize. Second, we determine a cohort of genes marked by PRC and elongating RNAPII (S5p(+)S7p(+)S2p(+); they create mRNA and protein, and their expression increases on PRC1 knockdown. We show that this group of PRC targets switches concerning energetic and PRC-repressed states within the ESC population, and that numerous havePI3Kγ roles in metabolic process.