ArticleCell reports2014
Targeting polycomb to pericentric heterochromatin in embryonic stem cells reveals a role for H2AK119u1 in PRC2 recruitment.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.
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Who cites it
206 citing papers in PubMed, 327 citations in OpenAlex.
- Divergent medulloblastoma chromatin states disclose KDM2B as a selective dependency.Nature genetics · 2026Article
- Epigenetic maintenance of PRC2-repressed chromatin requires RTT109 but not H3K56 acetylation.PLoS genetics · 2026Article
- Hierarchical chromatin polyvalency governs robust gene regulation and organogenesis.bioRxiv : the preprint server for biology · 2026Article
- Polycomb Group Proteins inBiology · 2026Review
- Loss of the USP22 deubiquitylase confers resistance to chemotherapy in small cell lung cancer.Nature communications · 2026Article
- Sustained PRC1.1 activity preserves gene repression independently of PRC2.2 and restrains leukemic cell differentiation.Nucleic acids research · 2026Article
- Developmental stage dominates cell-type identity and reveals a chromatin regulatory function for Rad50 in Drosophila.Nucleic acids research · 2026Article
- Protease-mediated PRC1 dissociation promotes H2AK119ub remodeling during stress responses.The EMBO journal · 2026Article
- Self-clustering of three CBX2 molecules drives PRC2 to promote facultative heterochromatinization of Polycomb target genes.Molecular cell · 2026Article
- Polycomb repressive-deubiquitinase complex safeguards oocyte epigenome and female fertility by restraining Polycomb activity.Nature communications · 2026Article
- EPOP restricts PRC2.1 targeting to chromatin by directly modulating enzyme complex dimerization.Nature communications · 2026Article
- Constitutive heterochromatin controls nuclear mechanics, morphology, and integrity through H3K9me3 mediated chromocenter compaction.Nucleus (Austin, Tex.) · 2025Article
- Synergistic function of RNA modifications inaBIOTECH · 2025Article
- Widespread association of Polycomb complex-deposited histone H2A monoubiquitylation with enhancers and neuronal gene regulation.Science advances · 2025Article
- Addressing the specific roles of histone modifications in transcriptional repression.Nature communications · 2025Article
- HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Analysis of a BCOR internal tandem duplication in mouse embryonic stem cell to neuronal precursor differentiation.Genetics · 2025Article
- Polycomb repressive complexes 1 and 2 independently and dynamically regulate euchromatin during cerebellar neurodevelopment.PLoS genetics · 2025Article
- Emerging Functions of the Repeat Genome in Nuclear Structure: A View from the Human Karyotype.Annual review of genomics and human genetics · 2025Review
- Analysis of histone modification interplay reveals two distinct domains in facultative heterochromatin in Pyricularia oryzae.Communications biology · 2025Article
146 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The mechanisms by which the major Polycomb group (PcG) complexes PRC1 and PRC2 are recruited to target sites in vertebrate cells are not well understood. Building on recent studies that determined a reciprocal relationship between DNA methylation and Polycomb activity, we demonstrate that, in methylation-deficient embryonic stem cells (ESCs), CpG density combined with antagonistic effects of H3K9me3 and H3K36me3 redirects PcG complexes to pericentric heterochromatin and gene-rich domains. Surprisingly, we find that PRC1-linked H2A monoubiquitylation is sufficient to recruit PRC2 to chromatin in vivo, suggesting a mechanism through which recognition of unmethylated CpG determines the localization of both PRC1 and PRC2 at canonical and atypical target sites. We discuss our data in light of emerging evidence suggesting that PcG recruitment is a default state at licensed chromatin sites, mediated by interplay between CpG hypomethylation and counteracting H3 tail 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.