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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE255094 | GEO | 2026/02/01

REPOSITORIES: GEO

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

Project description: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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PRC2 primes bivalent target genes for transcription induction independent of histone methyltransferase activity [RNA-seq]

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

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Loss of Kmt2c or Kmt2d primes urothelium for tumorigenesis and redistributes KMT2A-menin to bivalent promoters.

Project description:Members of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation. Kmt2c/d knockout further led to KMT2A-menin redistribution from KMT2D localized enhancers to CpG-high and bivalent promoters, resulting in derepression of signal-induced immediate early genes. Therapeutically, Kmt2c/d knockout upregulated epidermal growth factor receptor signaling and conferred vulnerability to epidermal growth factor receptor inhibitors. Together, our data posit that functional loss of Kmt2c/d licenses a molecular 'field effect' priming histologically normal urothelium for oncogenic transformation and presents therapeutic vulnerabilities.

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Project description:Imprinted X-inactivation is a paradigm of transgenerational epigenetic inheritance in mammals and silences genes exclusively on the paternally-inherited X-chromosome. Here, we test the hypothesis that oocyte-derived maternal Polycomb repressive complex 2 (PRC2) protein EED orchestrates the selective inactivation of the paternal-X in mouse embryos. In maternal Eed null (Eedm-/-) but not zygotic Eed null female and male embryos, the maternal X-chromosome ectopically induced Xist lncRNA, which silences X-linked genes. Subsequently, Xist was silenced from one of the two X-chromosomes in females and from the sole maternal-X in males. As a result, later-stage female Eedm-/- embryos displayed random X-inactivation. The kinetics of Xist RNA induction in Eedm-/- embryos resemble that of early human embryos, which lack oocyte-derived PRC2 and only undergo random X-inactivation. Thus, expression of PRC2 genes in the oocyte and transmission of the gene products to the embryo may dictate the occurrence of imprinted X-inactivation in mammals.

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