Evidence map›Paper›PMID 23959865›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Establishing a hematopoietic genetic network through locus-specific integration of chromatin regulators.

Andrew W DeVilbiss, Meghan E Boyer, Emery H Bresnick

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 31 citations in OpenAlex.

  1. Pathogenic GATA2 genetic variants utilize an obligate enhancer mechanism to distort a multilineage differentiation program.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  10. DifferentialEnvironmental health perspectives · 2018
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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

3 authors at 1 institution in 1 country.

Andrew W DeVilbissDepartment of Cell and Regenerative Biology, Wisconsin Institutes for Medical Research, Carbone Cancer Center, University of Wisconsin-Madison Blood Research Program, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA.
Meghan E Boyer
Emery H Bresnick
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Transcriptional Control of Hemoglobin Synthesis and Erythrocyte DevelopmentR01DK050107 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI Emery H. Bresnick · 1996 to 2026
$6.1M
Transcriptional Control of Hemoglobin SynthesisR37DK050107 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI BRESNICK, EMERY H · 2011 to 2020
$3.5M
Graduate Training In Cellular And Molecular Pathogenesis Of Human DiseasesT32GM081061 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2010 to 2019
$1.8M
NCI NIH HHS P30 CA014520NIDDK NIH HHS DK50107NIDDK NIH HHS R01 DK050107NIDDK NIH HHS R37 DK050107NIGMS NIH HHS T32 GM081061
6 · The paper itself

Abstract

The establishment and maintenance of cell type-specific transcriptional programs require an ensemble of broadly expressed chromatin remodeling and modifying enzymes. Many questions remain unanswered regarding the contributions of these enzymes to specialized genetic networks that control critical processes, such as lineage commitment and cellular differentiation. We have been addressing this problem in the context of erythrocyte development driven by the transcription factor GATA-1 and its coregulator Friend of GATA-1 (FOG-1). As certain GATA-1 target genes have little to no FOG-1 requirement for expression, presumably additional coregulators can mediate GATA-1 function. Using a genetic complementation assay and RNA interference in GATA-1-null cells, we demonstrate a vital link between GATA-1 and the histone H4 lysine 20 methyltransferase PR-Set7/SetD8 (SetD8). GATA-1 selectively induced H4 monomethylated lysine 20 at repressed, but not activated, loci, and endogenous SetD8 mediated GATA-1-dependent repression of a cohort of its target genes. GATA-1 used different combinations of SetD8, FOG-1, and the FOG-1-interacting nucleosome remodeling and deacetylase complex component Mi2β to repress distinct target genes. Implicating SetD8 as a context-dependent GATA-1 corepressor expands the repertoire of coregulators mediating establishment/maintenance of the erythroid cell genetic network, and provides a biological framework for dissecting the cell type-specific functions of this important coregulator. We propose a coregulator matrix model in which distinct combinations of chromatin regulators are required at different GATA-1 target genes, and the unique attributes of the target loci mandate these combinations.

Indexed as

Gene Expression RegulationGene Regulatory NetworksAnimalsCell Line, TumorCells, CulturedCHO CellsChromatinCricetinaeCricetulusErythroid CellsGATA1 Transcription FactorGene Expression ProfilingHematopoietic Stem CellsHistone-Lysine N-MethyltransferaseMi-2 Nucleosome Remodeling and Deacetylase ComplexMiceChromatinGata1 protein, mouseGATA1 Transcription FactorHistone-Lysine N-MethyltransferaseKMT5a protein, mouseMi-2 Nucleosome Remodeling and Deacetylase ComplexNuclear ProteinsTranscription FactorsZfpm1 protein, mouseepigeneticserythroidGATAgenomics

Identifiers

PMID23959865
PMCPMC3767509
OpenAlexW1963941240

What OpenQuestion holds

Textmetadata
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.