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PRC2 primes bivalent target genes for transcription induction independent of histone methyltransferase activity [ChIP-seq]

GSE255093 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2026/02/01 Platform GPL24247
Summary
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.
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Also filed as BioProject PRJNA1073506 and SRA study SRP488228. Searching any of these in the dataset finder brings you back here.

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