Synergy between Variant PRC1 Complexes Defines Polycomb-Mediated Gene Repression
Open accessAbstract
The Polycomb system modifies chromatin and plays an essential role in repressing gene expression to control normal mammalian development. However, the components and mechanisms that define how Polycomb protein complexes achieve this remain enigmatic. Here, we use combinatorial genetic perturbation coupled with quantitative genomics to discover the central determinants of Polycomb-mediated gene repression in mouse embryonic stem cells. We demonstrate that canonical Polycomb repressive complex 1 (PRC1), which mediates higher-order chromatin structures, contributes little to gene repression. Instead, we uncover an unexpectedly high degree of synergy between variant PRC1 complexes, which is fundamental to gene repression. We further demonstrate that variant PRC1 complexes are responsible for distinct pools of H2A monoubiquitylation that are associated with repression of Polycomb target genes and silencing during X chromosome inactivation. Together, these discoveries reveal a new variant PRC1-dependent logic for Polycomb-mediated gene repression.
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ChIP-seq bigwigs were generated with scaling factors calculated using the formula (human reads in input) / (mouse reads in input) / (human reads in ChIP) x 15,000,000 to calibrate between mouse ESCs and human HEK spike-in.
“Bigwigs were generated with the bamCoverage function from deepTools (82) with scaling factors calculated using the formula (human reads in input) / (mouse reads in input) / (human reads in ChIP) x 15000000 (83, 84).”
From Synergy between regulatory elements can render cohesin dispensable for distal enhancer function (2026) · cites this paper as [84]
The STAR Methods (Quantification and Statistical Analysis; page unavailable) give the same spike-in-to-mouse input read ratio divided by spike-in ChIP reads, and the Method Details identify human HEK293T cells as the spike-in for cross-linked ChIP-seq in mouse ESCs. However, the source uses a coefficient α chosen so the largest downsampling factor equals 1, not a fixed multiplier of 15,000,000; it also describes subsampling reads rather than generating bigWigs with bamCoverage. (LLM, conf=0.88)
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- Authors
- Fursova, N. A., Blackledge, N. P., Nakayama, M., Ito, S., Koseki, Y., Farcas, A. M., King, H. W., Koseki, H., & Klose, R. J.
- Affiliations
- University of Oxford (GB)
- Kazusa DNA Research Institute (JP)
- RIKEN Center for Integrative Medical Sciences (JP)
- Japan Agency for Medical Research and Development (JP)
- Corresponding author
- Klose, Robert J.
- ORCID
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2019-06
- Volume
- 74
- Issue
- 5
- Pages
- 1020-1036.e8
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC6561741
- OpenAlex
- W2941917579
- Cited by
- 267
- References
- 114
- Citations by year
- 2026: 25 · 2025: 35 · 2024: 35 · 2023: 30 · 2022: 39 · 2021: 44 · 2020: 42 · 2019: 16
- FWCI
- 11.66
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Funders
- European Research Council (681440)
- Lister Institute of Preventive Medicine
- Wellcome Trust (209400/Z/17/Z)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- PRC1, X chromosome inactivation, mouse embryonic stem cells, chromatin modification, quantitative genomics, higher-order chromatin structure
- MeSH terms
- Mouse Embryonic Stem Cells, Animals, Chromatin, Histones, Genomics, RNA Interference, X Chromosome Inactivation, Mice, Ubiquitination, Polycomb Repressive Complex 1
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