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PRC2 primes bivalent target genes for transcription induction independent of histone methyltransferase activity [ChIP-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: GSE255093 | GEO | 2026/02/01

REPOSITORIES: GEO

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

2026-02-01 | GSE255094 | GEO

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

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

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

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

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Two faces of bivalent domain regulate VEGFA responsiveness and angiogenesis

Project description:The bivalent domain at promoter region is a unique epigenetic feature poised for activation or repression during cell differentiation in embryonic stem cell. However, the function of bivalent domains in already differentiated cells remains exclusive. By profiling the epigenetic landscape of endothelial cells during VEGFA stimulation, we discovered that bivalent domains are widespread in endothelial cells and preferentially marked genes responsive to VEGFA. The bivalent domains responsive to VEGFA have more permissive chromatin environment comparing to other bivalent domains. The initial activation of bivalent genes depends on RNAPII pausing release induced by EZH1 rather than removal of H3K27me3. The later suppression of bivalent gene expression depended on KDM5A recruitment by its interaction with PRC2. Importantly, EZH1 promoted both in vitro and in vivo angiogenesis by upregulating EGR3, whereas KDM5A dampened angiogenesis. Collectively, this study demonstrated a novel dual function of bivalent domains in endothelial cells to control VEGF responsiveness and angiogenesis.

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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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ERK potentiates transactivation and oncogenic function of ERG by phosphorylation induced dissociation of PRC2 complex

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Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency [ChIP-Seq]

Project description:Here we report that NONO, a nuclear para-speckle component, instead functions as a chromatin regulator in mESCs acting in the ERK signaling pathway to regulate the balance between ground state versus mESCs primed for differentiation. NONO loss increases a \u201cground-like\u201d population of mESCs favoring self-renewal and more resist to differentiation, partially mimicking the effects of 2i. Mechanistically, NONO and ERK mainly co-binds a subset of development related, bivalent genes. Importantly, NONO and ERK reciprocally regulate one another, i.e. NONO regulates ERK activation while ERK controls NONO chromatin association, forming a self-reinforcing feedback loop. Our findings thus reveal a cell intrinsic mechanism involving NONO and ERK, which impact the balance between self-renewal and differentiation, respectively.

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Nono, a novel bivalent domain factor, regulates Erk signaling and mouse embryonic stem cell pluripotency [RNA-Seq]

Project description:Here we report that Nono instead functions as a chromatin regulator cooperating with Erk to regulate mESC pluripotency. We demonstrate that Nono loss leads to robust self-renewing mESCs with enhanced expression of Nanog and Klf4, epigenome and transcriptome re-patterning to a “ground-like state” with global reduction of H3K27me3 and DNA methylation resembling the Erk inhibitor PD03 treated mESCs and 2i (both GSK and Erk kinase inhibitors)-induced “ground state”. Mechanistically, Nono and Erk co-bind at a subset of development-related, bivalent genes. Ablation of Nono compromises Erk activation and RNA polymerase II C-terminal Domain serine 5 phosphorylation, and while inactivation of Erk evicts Nono from chromatin, revealing reciprocal regulation. Furthermore, Nono loss results in a compromised activation of its target bivalent genes upon differentiation and the differentiation itself. These findings reveal an unanticipated role of Nono in collaborating with Erk signaling to regulate the integrity of bivalent domain and mESC pluripotency.

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Switching from Random to Imprinted X-inactivation by Maternal PRC2

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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Project description:Characterisation of a new subgroup of DMG lacking H3-K27M mutation that is defined by H3K27me3 loss and EZHIP overexpression that can be detected by IHC. These tumors are distinct from EZHIP-positive posterior fossa ependymomas and are associated with a dismal prognosis. We propose that these EZHIP/H3-WT tumors need to be considered similar to canonical DIPG/DMG, thus extending the spectrum of DMG with PRC2 inhibition beyond H3-K27M mutation

2020-03-20 | E-MTAB-8888 | biostudies-arrayexpress

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