Evidence map›Paper›PMID 31029541›Full record

ArticleMolecular cell2019

Synergy between Variant PRC1 Complexes Defines Polycomb-Mediated Gene Repression.

Nadezda A Fursova, Neil P Blackledge, Manabu Nakayama, Shinsuke Ito, Yoko Koseki, Anca M Farcas, Hamish W King, Haruhiko Koseki, Robert J Klose

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed
14.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

171 citing papers in PubMed, 284 citations in OpenAlex.

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  7. Polycomb-mediated 3D chromatin interactions in gene regulation.Current opinion in genetics & development · 2026
    Review
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  18. PRC1-Mediated H2Aub Loop Formation and Function in Arabidopsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  19. Article
  20. Article

111 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Nadezda A FursovaDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Neil P BlackledgeDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Manabu NakayamaLaboratory of Medical Omics Research, Department of Frontier Research and Development, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu, Chiba 292-0818, Japan.
Shinsuke ItoLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, 1-7-29 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
Yoko KosekiLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, 1-7-29 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
Anca M FarcasDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Hamish W KingDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.
Haruhiko KosekiLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, 1-7-29 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan; AMED-CREST, Japanese Agency for Medical Research and Development, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.
Robert J KloseDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK. Electronic address: rob.klose@bioch.ox.ac.uk.
University of Oxford · GBRIKEN Center for Integrative Medical Sciences · JPKazusa DNA Research Institute · JP

Funding

Wellcome Trust
6 · The paper itself

Abstract

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.

Indexed as

GenomicsAnimalsChromatinHistonesMiceMouse Embryonic Stem CellsPolycomb Repressive Complex 1RNA InterferenceUbiquitinationX Chromosome InactivationChromatingamma-H2AX protein, mouseHistonesPolycomb Repressive Complex 1chromatinepigeneticsgene expressionhistonehistone modificationPCGFpolycombPRC1PRC2ubiquitylation

Identifiers

PMID31029541
PMCPMC6561741
OpenAlexW2941917579

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.