Evidence map›Paper›PMID 30609396›Full record

ArticleCell stem cell2019

The BAF and PRC2 Complex Subunits Dpf2 and Eed Antagonistically Converge on Tbx3 to Control ESC Differentiation.

Wensheng Zhang, Constantinos Chronis, Xi Chen, Heyao Zhang, Rapolas Spalinskas, Mercedes Pardo, Liangliang Chen, Guangming Wu, Zhexin Zhu, Yong Yu and 7 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell stem cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

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  18. Regulation of Embryonic Stem Cell Self-Renewal.Life (Basel, Switzerland) · 2022
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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

17 authors at 8 institutions in 5 countries.

Wensheng ZhangCam-Su Genomic Resource Center, Soochow University, Suzhou 215123, China; Wellcome Sanger Institute, Hinxton CB10 1SA, UK. Electronic address: zhangwensheng@suda.edu.cn.
Constantinos ChronisDepartment of Biological Chemistry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California Los Angeles, Los Angeles, CA, USA; Bioinformatics Program, Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, University of California Los Angeles, Los Angeles, CA 90095, USA.
Xi ChenWellcome Sanger Institute, Hinxton CB10 1SA, UK.
Heyao ZhangCam-Su Genomic Resource Center, Soochow University, Suzhou 215123, China.
Rapolas SpalinskasScience for Life Laboratory, Division of Gene Technology, KTH Royal Institute of Technology, 106 91 Stockholm, Sweden.
Mercedes PardoThe Institute of Cancer Research, Chester Beatty Laboratories, London, UK.
Liangliang ChenCam-Su Genomic Resource Center, Soochow University, Suzhou 215123, China.
Guangming WuDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstrasse 20, 48149 Münster, Germany.
Zhexin ZhuWellcome Sanger Institute, Hinxton CB10 1SA, UK.
Yong YuWellcome Sanger Institute, Hinxton CB10 1SA, UK.
Lu YuThe Institute of Cancer Research, Chester Beatty Laboratories, London, UK.
Jyoti ChoudharyThe Institute of Cancer Research, Chester Beatty Laboratories, London, UK.
Jennifer NicholsWellcome Trust - Medical Research Council Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK.
Mana M ParastDepartment of Pathology, University of California, San Diego, La Jolla, CA, USA; Sanford Consortium for Regenerative Medicine, University of California, San Diego, La Jolla, CA, USA.
Boris GreberDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstrasse 20, 48149 Münster, Germany.
Pelin SahlénScience for Life Laboratory, Division of Gene Technology, KTH Royal Institute of Technology, 106 91 Stockholm, Sweden.
Kathrin PlathDepartment of Biological Chemistry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California Los Angeles, Los Angeles, CA, USA; Bioinformatics Program, Jonsson Comprehensive Cancer Center, University of California Los Angeles, Los Angeles, CA, USA; Molecular Biology Institute, University of California Los Angeles, Los Angeles, CA 90095, USA.
Institute of Cancer Research · GBSoochow University · CNWellcome Sanger Institute · GBKTH Royal Institute of Technology · SEMax Planck Institute for Molecular Biomedicine · DEUniversity of California, Los Angeles · USSanford Consortium for Regenerative Medicine · USWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Roles of sumoylation and alternative polyadenylation in cellular reprogrammingP01GM099134 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PLATH, KATHRIN · 2011 to 2021
$20.3M
Howard Hughes Medical InstituteMedical Research Council MC_PC_12009NIGMS NIH HHS P01 GM099134Wellcome Trust
6 · The paper itself

Abstract

BAF complexes are composed of different subunits with varying functional and developmental roles, although many subunits have not been examined in depth. Here we show that the Baf45 subunit Dpf2 maintains pluripotency and ESC differentiation potential. Dpf2 co-occupies enhancers with Oct4, Sox2, p300, and the BAF subunit Brg1, and deleting Dpf2 perturbs ESC self-renewal, induces repression of Tbx3, and impairs mesendodermal differentiation without dramatically altering Brg1 localization. Mesendodermal differentiation can be rescued by restoring Tbx3 expression, whose distal enhancer is positively regulated by Dpf2-dependent H3K27ac maintenance and recruitment of pluripotency TFs and Brg1. In contrast, the PRC2 subunit Eed binds an intragenic Tbx3 enhancer to oppose Dpf2-dependent Tbx3 expression and mesendodermal differentiation. The PRC2 subunit Ezh2 likewise opposes Dpf2-dependent differentiation through a distinct mechanism involving Nanog repression. Together, these findings delineate distinct mechanistic roles for specific BAF and PRC2 subunits during ESC differentiation.

Indexed as

Cell DifferentiationAnimalsApoptosisCell CycleDNA-Binding ProteinsEmbryonic Stem CellsHistonesMiceMice, KnockoutNanog Homeobox ProteinPolycomb Repressive Complex 2Protein SubunitsT-Box Domain ProteinsTranscription FactorsDNA-Binding ProteinsDPF2 protein, mouseEed protein, mouseHistonesNanog Homeobox ProteinNanog protein, mousePolycomb Repressive Complex 2Protein SubunitsT-Box Domain ProteinsTbx3 protein, mouseTranscription FactorsBAF complexcell fate decisiondifferentiationembryonic stem cellsenhancershistone modificationpluripotencyPRC2 complexself-renewal

Identifiers

PMID30609396
PMCPMC6486830
OpenAlexW2907699911

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.