Evidence map›Paper›PMID 34117481›Full record

ArticleNature structural & molecular biology2021

mSWI/SNF promotes Polycomb repression both directly and through genome-wide redistribution.

Christopher M Weber, Antonina Hafner, Jacob G Kirkland, Simon M G Braun, Benjamin Z Stanton, Alistair N Boettiger, Gerald R Crabtree

Open access · greenAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 86 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

7 authors at 5 institutions in 2 countries.

Christopher M WeberDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Antonina HafnerDevelopmental Biology, Stanford University School of Medicine, Stanford, CA, USA.
Jacob G KirklandDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-5617-7065
Simon M G BraunDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-2622-9914
Benjamin Z StantonNationwide Children's Hospital, Center for Childhood Cancer and Blood Diseases, Columbus, OH, USA.ORCID http://orcid.org/0000-0002-2613-2955
Alistair N BoettigerDevelopmental Biology, Stanford University School of Medicine, Stanford, CA, USA.
Gerald R CrabtreeDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA. crabtree@stanford.edu.ORCID http://orcid.org/0000-0001-9685-7911
Stanford University · USHoward Hughes Medical Institute · USNationwide Children's Hospital · USOklahoma Medical Research Foundation · USUniversity of Geneva · CH

Funding

ATP-Dependent Chromatin Remodeling in Human MalignancyR01CA163915 · NCI · STANFORD UNIVERSITY · PI Gerald R. Crabtree · 2012 to 2026
$5.4M
ATP-Dependent Chromatin Regulation in Neurodevelopment and Human DiseaseR37NS046789 · NINDS · STANFORD UNIVERSITY · PI CRABTREE, GERALD R. · 2013 to 2019
$2.7M
High resolution imaging of genome structure and gene regulation in developmentDP2GM132935 · NIGMS · STANFORD UNIVERSITY · PI BOETTIGER, ALISTAIR N. · 2018 to 2018
$2.3M
HIJACKING CANCER DRIVERS TO ACTIVATE PROAPOPTOTIC GENES IN DLBCLR01CA276167 · NCI · STANFORD UNIVERSITY · PI Gerald R. Crabtree, NATHANAEL Schiander GRAY · 2023 to 2026
$2.2M
Small molecule regulation of endogenous transcription factors for circuit-specific neuromodulationRF1MH126720 · NIMH · STANFORD UNIVERSITY · PI CRABTREE, GERALD R. · 2021 to 2021
$1.3M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA163915NCI NIH HHS R01 CA276167NIGMS NIH HHS DP2 GM132935NIMH NIH HHS RF1 MH126720NINDS NIH HHS R37 NS046789
6 · The paper itself

Abstract

The mammalian SWI/SNF complex, or BAF complex, has a conserved and direct role in antagonizing Polycomb-mediated repression. Yet, BAF also promotes repression by Polycomb in stem cells and cancer. How BAF both antagonizes and promotes Polycomb-mediated repression remains unknown. Here, we utilize targeted protein degradation to dissect the BAF-Polycomb axis in mouse embryonic stem cells on short timescales. We report that rapid BAF depletion redistributes Polycomb repressive complexes PRC1 and PRC2 from highly occupied domains, like Hox clusters, to weakly occupied sites normally opposed by BAF. Polycomb redistribution from highly repressed domains results in their decompaction, gain of active epigenomic features and transcriptional derepression. Surprisingly, through dose-dependent degradation of PRC1 and PRC2, we identify a conventional role for BAF in Polycomb-mediated repression, in addition to global Polycomb redistribution. These findings provide new mechanistic insight into the highly dynamic state of the Polycomb-Trithorax axis.

Indexed as

AnimalsCells, CulturedChromatin Assembly and DisassemblyCRISPR-Cas SystemsDNA-Binding ProteinsDNA HelicasesEmbryonic Stem CellsEpigenesis, GeneticEpigenetic RepressionGene EditingGene Expression RegulationGenes, HomeoboxGenomeHEK293 CellsHomeodomain ProteinsHumansDNA-Binding ProteinsDNA HelicasesHomeodomain ProteinsMultiprotein ComplexesNuclear ProteinsPolycomb-Group ProteinsRecombinant Fusion ProteinsSmarca4 protein, mouseTranscription Factors

Identifiers

PMID34117481
PMCPMC8504423
OpenAlexW3165925524

What OpenQuestion holds

Textmetadata
LicenceTDM
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.