Evidence map›Paper›PMID 32270030›Full record

ArticleScience advances2020

Parallel PRC2/cPRC1 and vPRC1 pathways silence lineage-specific genes and maintain self-renewal in mouse embryonic stem cells.

J A Zepeda-Martinez, C Pribitzer, J Wang, D Bsteh, S Golumbeanu, Q Zhao, T R Burkard, B Reichholf, S K Rhie, J Jude and 3 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

J A Zepeda-MartinezInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0002-3192-3153
C PribitzerInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.
J WangResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0002-0127-501X
D BstehInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0002-0405-0641
S GolumbeanuDepartment of Biochemistry and Molecular Medicine, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0003-3257-9902
Q ZhaoDepartment of Biochemistry and Molecular Medicine, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-0651-2643
T R BurkardInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0002-0884-2929
B ReichholfInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.
S K RhieDepartment of Biochemistry and Molecular Medicine, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-5522-5296
J JudeResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0002-9091-9867
H F MoussaInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0003-3463-0126
J ZuberResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0001-8810-6835
O BellInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), 1030 Vienna, Austria.ORCID 0000-0002-7639-5948
Institute of Molecular Biotechnology · ATUniversity of Southern California · USResearch Institute of Molecular Pathology · AT

Funding

Identification and Clinical Validation of Key Transcription Factor Isoforms Linked to Breast and Prostate Cancer Subgroups using Epigenetic TraitsK01CA229995 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RHIE, SUHN KYONG · 2018 to 2020
$637k
NCI NIH HHS K01 CA229995
6 · The paper itself

Abstract

The transcriptional repressors Polycomb repressive complex 1 (PRC1) and PRC2 are required to maintain cell fate during embryonic development. PRC1 and PRC2 catalyze distinct histone modifications, establishing repressive chromatin at shared targets. How PRC1, which consists of canonical PRC1 (cPRC1) and variant PRC1 (vPRC1) complexes, and PRC2 cooperate to silence genes and support mouse embryonic stem cell (mESC) self-renewal is unclear. Using combinatorial genetic perturbations, we show that independent pathways of cPRC1 and vPRC1 are responsible for maintenance of H2A monoubiquitylation and silencing of shared target genes. Individual loss of PRC2-dependent cPRC1 or PRC2-independent vPRC1 disrupts only one pathway and does not impair mESC self-renewal capacity. However, loss of both pathways leads to mESC differentiation and activation of a subset of lineage-specific genes co-occupied by relatively high levels of PRC1/PRC2. Thus, parallel pathways explain the differential requirements for PRC1 and PRC2 and provide robust silencing of lineage-specific genes.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsCell DifferentiationCell LineageCell Self RenewalGene SilencingMiceModels, BiologicalMouse Embryonic Stem CellsPolycomb Repressive Complex 1Polycomb Repressive Complex 2Polycomb Repressive Complex 1Polycomb Repressive Complex 2

Identifiers

PMID32270030
PMCPMC7112768
OpenAlexW3014935454

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.