Evidence map›Paper›PMID 27150236›Full record

ArticleStem cell reports2016

MicroRNAs of the miR-290-295 Family Maintain Bivalency in Mouse Embryonic Stem Cells.

Bryony Graham, Antoine Marcais, Gopuraja Dharmalingam, Thomas Carroll, Chryssa Kanellopoulou, Johannes Graumann, Tatyana B Nesterova, Anna Bermange, Pijus Brazauskas, Barbara Xella and 6 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  16. Deciphering the Epigenetic Code in Embryonic and Dental Pulp Stem Cells.The Yale journal of biology and medicine · 2016
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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

16 authors at 6 institutions in 3 countries.

Bryony GrahamLymphocyte Development Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; Epigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; MRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
Antoine MarcaisLymphocyte Development Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; Epigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Gopuraja DharmalingamEpigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Thomas CarrollEpigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Chryssa KanellopoulouLaboratory of Immunology, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA.
Johannes GraumannDepartment of Proteomics and Signal Transduction, Max-Planck Institute for Biochemistry, 82152 Martinsried, Germany.
Tatyana B NesterovaDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Anna BermangeLymphocyte Development Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; Epigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Pijus BrazauskasLudwig Institute for Cancer Research, University of Oxford, Nuffield Department of Clinical Medicine, Oxford OX3 7DQ, UK.
Barbara XellaMRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
Skirmantas KriaucionisLudwig Institute for Cancer Research, University of Oxford, Nuffield Department of Clinical Medicine, Oxford OX3 7DQ, UK.
Douglas R HiggsMRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.
Neil BrockdorffDepartment of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Matthias MannDepartment of Proteomics and Signal Transduction, Max-Planck Institute for Biochemistry, 82152 Martinsried, Germany.
Amanda G FisherLymphocyte Development Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; Epigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.
Matthias MerkenschlagerLymphocyte Development Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK; Epigenetics Section, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK. Electronic address: matthias.merkenschlager@csc.mrc.ac.uk.
Imperial College London · GBUniversity of Oxford · GBLudwig Cancer Research · GBMax Planck Institute of Biochemistry · DEMRC Weatherall Institute of Molecular Medicine · GBNational Institutes of Health · US

Funding

Medical Research Council MC_U120027516
6 · The paper itself

Abstract

Numerous developmentally regulated genes in mouse embryonic stem cells (ESCs) are marked by both active (H3K4me3)- and polycomb group (PcG)-mediated repressive (H3K27me3) histone modifications. This bivalent state is thought to be important for transcriptional poising, but the mechanisms that regulate bivalent genes and the bivalent state remain incompletely understood. Examining the contribution of microRNAs (miRNAs) to the regulation of bivalent genes, we found that the miRNA biogenesis enzyme DICER was required for the binding of the PRC2 core components EZH2 and SUZ12, and for the presence of the PRC2-mediated histone modification H3K27me3 at many bivalent genes. Genes that lost bivalency were preferentially upregulated at the mRNA and protein levels. Finally, reconstituting Dicer-deficient ESCs with ESC miRNAs restored bivalent gene repression and PRC2 binding at formerly bivalent genes. Therefore, miRNAs regulate bivalent genes and the bivalent state itself.

Indexed as

AnimalsCell DifferentiationDEAD-box RNA HelicasesEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, DevelopmentalHistone CodeHistone-Lysine N-MethyltransferaseMiceMicroRNAsMouse Embryonic Stem CellsPolycomb Repressive Complex 2Promoter Regions, GeneticRibonuclease IIITranscriptional ActivationDEAD-box RNA HelicasesDicer1 protein, mouseEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseHistone-Lysine N-MethyltransferaseMicroRNAsMIRN290 microRNA, mouseMIRN295 microRNA, mousePolycomb Repressive Complex 2Ribonuclease IIISuz12 protein, mouse

Identifiers

PMID27150236
PMCPMC4939759
OpenAlexW2341512691

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.