Evidence map›Paper›PMID 26804911›Full record

ArticleCell reports2016

H2A.Z.1 Monoubiquitylation Antagonizes BRD2 to Maintain Poised Chromatin in ESCs.

Lauren E Surface, Paul A Fields, Vidya Subramanian, Russell Behmer, Namrata Udeshi, Sally E Peach, Steven A Carr, Jacob D Jaffe, Laurie A Boyer

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.7field-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

45 citing papers in PubMed, 76 citations in OpenAlex.

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  16. Zebrafish ParalogsJournal of developmental biology · 2021
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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

9 authors at 2 institutions in 1 country.

Lauren E SurfaceDepartment of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139 USA.
Paul A FieldsDepartment of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139 USA.
Vidya SubramanianDepartment of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139 USA.
Russell BehmerDepartment of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139 USA.
Namrata UdeshiBroad Institute, 7 Cambridge Center, Cambridge, MA 02142, USA.
Sally E PeachBroad Institute, 7 Cambridge Center, Cambridge, MA 02142, USA.
Steven A CarrBroad Institute, 7 Cambridge Center, Cambridge, MA 02142, USA.
Jacob D JaffeBroad Institute, 7 Cambridge Center, Cambridge, MA 02142, USA.
Laurie A BoyerDepartment of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139 USA. Electronic address: lboyer@mit.edu.
Massachusetts Institute of Technology · USBroad Institute · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
The Epigenetic Landscape of Heart DevelopmentU01HL098179 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI BOYER, LAURIE A, BRUNEAU, BENOIT GAETAN · 2009 to 2014
$10.0M
NCI NIH HHS P30-CA14051NHLBI NIH HHS U01 HL098179NHLBI NIH HHS U01HL098179NIGMS NIH HHS T32 GM007287NIGMS NIH HHS T32GM007287
6 · The paper itself

Abstract

Histone variant H2A.Z occupies the promoters of active and poised, bivalent genes in embryonic stem cells (ESCs) to regulate developmental programs, yet how it contributes to these contrasting states is poorly understood. Here, we investigate the function of H2A.Z.1 monoubiquitylation (H2A.Z.1ub) by mutation of the PRC1 target residues (H2A.Z.1(K3R3)). We show that H2A.Z.1(K3R3) is properly incorporated at target promoters in murine ESCs (mESCs), but loss of monoubiquitylation leads to de-repression of bivalent genes, loss of Polycomb binding, and faulty lineage commitment. Using quantitative proteomics, we find that tandem bromodomain proteins, including the BET family member BRD2, are enriched in H2A.Z.1 chromatin. We further show that BRD2 is gained at de-repressed promoters in H2A.Z.1(K3R3) mESCs, whereas BRD2 inhibition restores gene silencing at these sites. Together, our study reveals an antagonistic relationship between H2A.Z.1ub and BRD2 to regulate the transcriptional balance at bivalent genes to enable proper execution of developmental programs.

Indexed as

UbiquitinationAnimalsBromodomain Containing ProteinsCell DifferentiationCell LineageCell Self RenewalChromatinChromosomal Proteins, Non-HistoneGene Expression Regulation, DevelopmentalHistonesMiceMouse Embryonic Stem CellsPolycomb-Group ProteinsPromoter Regions, GeneticProtein BindingTranscription FactorsBrd2 protein, mouseBromodomain Containing ProteinsChromatinChromosomal Proteins, Non-HistoneH2az1 protein, mouseHistonesPolycomb-Group ProteinsTranscription Factors

Identifiers

PMID26804911
PMCPMC4764991
OpenAlexW2272736557

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.