ArticleMolecular cell2023
PRC2.1- and PRC2.2-specific accessory proteins drive recruitment of different forms of canonical PRC1.
Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 69 citations in OpenAlex.
- Hierarchical chromatin polyvalency governs robust gene regulation and organogenesis.bioRxiv : the preprint server for biology · 2026Article
- Inhibition of USP7 Destabilizes the Noncanonical PRC1.1 Complex and Induces Neuroblastoma Differentiation.Molecular cancer research : MCR · 2026Article
- Polycomb-mediated 3D-genome organization controls replication timing.Science advances · 2026Article
- Sustained PRC1.1 activity preserves gene repression independently of PRC2.2 and restrains leukemic cell differentiation.Nucleic acids research · 2026Article
- Long-term maintenance of H3K27me3 in postmitotic neurons is dispensable for gene expression regulation.bioRxiv : the preprint server for biology · 2026Article
- The RNA binding protein LIN28A mediates chromatin dynamics during neuronal differentiation.Cell death and differentiation · 2026Article
- Polycomb-mediated 3D chromatin interactions in gene regulation.Current opinion in genetics & development · 2026Review
- Self-clustering of three CBX2 molecules drives PRC2 to promote facultative heterochromatinization of Polycomb target genes.Molecular cell · 2026Article
- Comparison with Ezh2 reveals the PRC2-dependent functions of Jarid2 in hematopoietic stem Cell lineage commitment.Stem cell reports · 2026Article
- Unbalanced chromatin binding of Polycomb complexes drives neurodevelopmental disorders.Molecular cell · 2026Article
- Emerging structural insights into PRC2 function in development and disease.Trends in biochemical sciences · 2026Review
- Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026Review
- 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
- Auto-inhibition of PRC2 by the broadly expressed long isoform of AEBP2.The EMBO journal · 2025Article
- Dominant-negative effects of Weaver syndrome-associated EZH2 variants.Genes & development · 2025Article
- Review
- HISTONE DEACETYLASE-1 is required for epigenome stability inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- EZH2 variants derived from cryptic splice sites govern distinct epigenetic patterns during embryonic development.Nucleic acids research · 2025Article
- Polycomb repressive complexes 1 and 2 independently and dynamically regulate euchromatin during cerebellar neurodevelopment.PLoS genetics · 2025Article
- Distinct specificity and functions of PRC2 subcomplexes in human stem cells and cardiac differentiation.Molecular cell · 2025Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycomb repressive complex 2 (PRC2) mediates H3K27me3 deposition, which is thought to recruit canonical PRC1 (cPRC1) via chromodomain-containing CBX proteins to promote stable repression of developmental genes. PRC2 forms two major subcomplexes, PRC2.1 and PRC2.2, but their specific roles remain unclear. Through genetic knockout (KO) and replacement of PRC2 subcomplex-specific subunits in naïve and primed pluripotent cells, we uncover distinct roles for PRC2.1 and PRC2.2 in mediating the recruitment of different forms of cPRC1. PRC2.1 catalyzes the majority of H3K27me3 at Polycomb target genes and is sufficient to promote recruitment of CBX2/4-cPRC1 but not CBX7-cPRC1. Conversely, while PRC2.2 is poor at catalyzing H3K27me3, we find that its accessory protein JARID2 is essential for recruitment of CBX7-cPRC1 and the consequent 3D chromatin interactions at Polycomb target genes. We therefore define distinct contributions of PRC2.1- and PRC2.2-specific accessory proteins to Polycomb-mediated repression and uncover a new mechanism for cPRC1 recruitment.
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