ArticleNature structural & molecular biology2025
Structural basis for the inhibition of PRC2 by active transcription histone posttranslational modifications.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Review
- Histone modification cross talk between a host and pathogen.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Polycomb Repressive Complex 2 (PRC2): A Context-Dependent Epigenetic Regulator of Brain Aging.Biomolecules · 2026Review
- Opposing function of AEBP2 isoforms fine-tune PRC2 catalytic activity.Nucleic acids research · 2026Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- Histone modification cross-talk: analytical tools and molecular mechanisms.The Biochemical journal · 2026Review
- The conserved N-terminal SANT1-binding domain (SBD) of EZH2 regulates PRC2 activity.Genes & development · 2026Article
- Hnf1aos1 as a Metabolic Coordinator of Hepatic Lipid Homeostasis and Feedback Control.Non-coding RNA · 2026Article
- Histone H4 acetyl-methyllysine marks accessible chromatin that resists compaction.bioRxiv : the preprint server for biology · 2026Article
- Endothelial-specific Ezh2 deficiency exacerbates blood-brain barrier dysfunction and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Emerging structural insights into PRC2 function in development and disease.Trends in biochemical sciences · 2026Review
- DOT1L provides transcriptional memory through PRC1.1 antagonism.Nature cell biology · 2026Article
- DNA methylation landscapes in human cells and their chromatin determinants.Ageing and cancer research & treatment · 2026Article
- Cancer-specific bivalent promoters featuring low-level H3K27me3 signals favor active transcription and govern the cancer cell state transition.Acta biochimica et biophysica Sinica · 2025Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Paraspeckle protein NONO regulates active chromatin by allosterically stimulating NSD1.Cell reports · 2025Article
- SETD2 suppresses tumorigenesis in a KRASeLife · 2025Article
Corrections and comments
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5 authors.
Funding
Abstract
Polycomb repressive complex 2 (PRC2) trimethylates histone H3 on K27 (H3K27me3) leading to gene silencing that is essential for embryonic development and maintenance of cell identity. PRC2 is regulated by protein cofactors and their crosstalk with histone modifications. Trimethylated histone H3 on K4 (H3K4me3) and K36 (H3K36me3) localize to sites of active transcription and inhibit PRC2 activity through unknown mechanisms. Using cryo-electron microscopy, we reveal that histone H3 tails containing H3K36me3 engage poorly with PRC2 and preclude its effective interaction with chromatin, while H3K4me3 binds to the allosteric site in the EED subunit, acting as an antagonist that competes with activators required for spreading of the H3K27me3 repressive mark. Thus, the location of the H3K4me3 and H3K36me3 modifications along the H3 tail allows them to target two requirements for efficient trimethylation of H3K27 by PRC2. We further show that the JARID2 cofactor modulates PRC2 activity in the presence of these histone modifications.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.