Evidence map›Paper›PMID 25250711›Full record

ArticleeLife2014

Polycomb- and REST-associated histone deacetylases are independent pathways toward a mature neuronal phenotype.

James C McGann, Jon A Oyer, Saurabh Garg, Huilan Yao, Jun Liu, Xin Feng, Lujian Liao, John R Yates, Gail Mandel

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  6. Heliyon · 2024
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  10. Review
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  13. The Genome-Wide Binding Profile for Human RE1 Silencing Transcription Factor Unveils a Unique Genetic Circuitry in Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
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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 4 institutions in 1 country.

James C McGannVollum Institute, Oregon Health and Science University, Portland, United States.
Jon A OyerVollum Institute, Oregon Health and Science University, Portland, United States.
Saurabh GargVollum Institute, Oregon Health and Science University, Portland, United States.
Huilan YaoVollum Institute, Oregon Health and Science University, Portland, United States.
Jun LiuVollum Institute, Oregon Health and Science University, Portland, United States.
Xin FengDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, United States.
Lujian LiaoDepartment of Chemical Physiology, Scripps Research Institute, La Jolla, United States.
John R YatesDepartment of Chemical Physiology, Scripps Research Institute, La Jolla, United States.
Gail MandelVollum Institute, Oregon Health and Science University, Portland, United States.
Howard Hughes Medical Institute · USOregon Health & Science University · USScripps Research Institute · USBaylor College of Medicine · US

Funding

TrainingP41GM103533 · NIGMS · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 2012 to 2021
$20.7M
REGULATION OF THE SODIUM CHANNEL IN EXCITABLE CELLSR01NS022518 · NINDS · TUFTS MEDICAL CENTER · PI MANDEL, GAIL · 1985 to 2013
$4.2M
Functional characterization of astrocytes in a mouse model of Rett syndromeF32NS078886 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MCGANN, JAMES · 2012 to 2013
$106k
Howard Hughes Medical InstituteNIGMS NIH HHS P41 GM103533NINDS NIH HHS NS078886NINDS NIH HHS NS22518
6 · The paper itself

Abstract

The bivalent hypothesis posits that genes encoding developmental regulators required for early lineage decisions are poised in stem/progenitor cells by the balance between a repressor histone modification (H3K27me3), mediated by the Polycomb Repressor Complex 2 (PRC2), and an activator modification (H3K4me3). In this study, we test whether this mechanism applies equally to genes that are not required until terminal differentiation. We focus on the RE1 Silencing Transcription Factor (REST) because it is expressed highly in stem cells and is an established global repressor of terminal neuronal genes. Elucidation of the REST complex, and comparison of chromatin marks and gene expression levels in control and REST-deficient stem cells, shows that REST target genes are poised by a mechanism independent of Polycomb, even at promoters which bear the H3K27me3 mark. Specifically, genes under REST control are actively repressed in stem cells by a balance of the H3K4me3 mark and a repressor complex that relies on histone deacetylase activity. Thus, chromatin distinctions between pro-neural and terminal neuronal genes are established at the embryonic stem cell stage by two parallel, but distinct, repressor pathways.

Indexed as

Cell DifferentiationAnimalsChromatinEmbryonic Stem CellsGene Expression RegulationHistone DeacetylasesHistonesLysineMethylationMiceNeuronsPhenotypePolycomb Repressive Complex 2Promoter Regions, GeneticRE1-Silencing Transcription FactorRepressor ProteinsChromatinHistone DeacetylasesHistonesLysinePolycomb Repressive Complex 2RE1-Silencing Transcription FactorRepressor Proteinschromosomesdevelopmental biologyES cellsgeneshistone deacetylasemouseneuronalpoisedPolycombRESTstem cells

Identifiers

PMID25250711
PMCPMC4371837
OpenAlexW2140067268

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.