PRC2 primes bivalent target genes for transcription induction independent of histone methyltransferase activity [ChIP-seq]
The loss of PRC2 results in decelerated kinetics of transcription induction of its target genes. Mechanistically, PRC2 deletion rather than its inactivation impairs ERK activity, and therefore leads to loss of phosphorylated RNA polymerase II (RNAPII) at serine-5, which is critical for rapid induction of bivalent genes. To further support these findings, ectopic expression of constitutively active ERK in PRC2-null embryonic stem cells partially restores transcription induction kinetics. Therefore, these findings propose a priming function of PRC2 in maintaining poised RNAPII and differentiation potential, extending its role beyond preserving cellular identity. Overall design: Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for the histone modification H3K27me3 and ERK2, RNAPII in WT and EZH2 KO ESCs.