Evidence map›Paper›PMID 26040698›Full record

ArticleNucleic acids research2015

A fine balance: epigenetic control of cellular quiescence by the tumor suppressor PRDM2/RIZ at a bivalent domain in the cyclin a gene.

Sirisha Cheedipudi, Deepika Puri, Amena Saleh, Hardik P Gala, Mohammed Rumman, Malini S Pillai, Prethish Sreenivas, Reety Arora, Jeeva Sellathurai, Henrik Daa Schrøder and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-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

26 citing papers in PubMed, 63 citations in OpenAlex.

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  15. Is There a Histone Code for Cellular Quiescence?Frontiers in cell and 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

12 authors at 3 institutions in 2 countries.

Sirisha CheedipudiInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Council of Scientific and Industrial Research-Centre for Cellular and Molecular Biology, Hyderabad 500 007, India Max Planck Institute for Heart and Lung Research, Bad Nauheim 61231, Germany.
Deepika PuriInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Max Planck Institute of Immunobiology and Epigenetics, Freiburg D-79108, Germany.
Amena SalehInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Manipal University, Manipal 576104 India.
Hardik P GalaInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Council of Scientific and Industrial Research-Centre for Cellular and Molecular Biology, Hyderabad 500 007, India.
Mohammed RummanInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Manipal University, Manipal 576104 India.
Malini S PillaiInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India.
Prethish SreenivasInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Council of Scientific and Industrial Research-Centre for Cellular and Molecular Biology, Hyderabad 500 007, India.
Reety AroraInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India.
Jeeva SellathuraiInstitute of Clinical Research, SDU Muscle Research Cluster (SMRC), University of Southern Denmark, Odense 5000 C, Denmark.
Henrik Daa SchrøderInstitute of Clinical Research, SDU Muscle Research Cluster (SMRC), University of Southern Denmark, Odense 5000 C, Denmark.
Rakesh K MishraCouncil of Scientific and Industrial Research-Centre for Cellular and Molecular Biology, Hyderabad 500 007, India.
Jyotsna DhawanInstitute for Stem Cell Biology and Regenerative Medicine, National Center for Biological Sciences, GKVK Post, Bellary Road, Bangalore 560065, India Council of Scientific and Industrial Research-Centre for Cellular and Molecular Biology, Hyderabad 500 007, India jdhawan@ncbs.res.in.
Institute for Stem Cell Biology and Regenerative Medicine · INUniversity of Southern Denmark · DKCouncil of Scientific and Industrial Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult stem cell quiescence is critical to ensure regeneration while minimizing tumorigenesis. Epigenetic regulation contributes to cell cycle control and differentiation, but few regulators of the chromatin state in quiescent cells are known. Here we report that the tumor suppressor PRDM2/RIZ, an H3K9 methyltransferase, is enriched in quiescent muscle stem cells in vivo and controls reversible quiescence in cultured myoblasts. We find that PRDM2 associates with >4400 promoters in G0 myoblasts, 55% of which are also marked with H3K9me2 and enriched for myogenic, cell cycle and developmental regulators. Knockdown of PRDM2 alters histone methylation at key promoters such as Myogenin and CyclinA2 (CCNA2), and subverts the quiescence program via global de-repression of myogenesis, and hyper-repression of the cell cycle. Further, PRDM2 acts upstream of the repressive PRC2 complex in G0. We identify a novel G0-specific bivalent chromatin domain in the CCNA2 locus. PRDM2 protein interacts with the PRC2 protein EZH2 and regulates its association with the bivalent domain in the CCNA2 gene. Our results suggest that induction of PRDM2 in G0 ensures that two antagonistic programs-myogenesis and the cell cycle-while stalled, are poised for reactivation. Together, these results indicate that epigenetic regulation by PRDM2 preserves key functions of the quiescent state, with implications for stem cell self-renewal.

Indexed as

Gene SilencingAdolescentAdultAnimalsCell Cycle CheckpointsCell DifferentiationCells, CulturedCyclin A2DNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinFemaleHistone-Lysine N-MethyltransferaseHumansIntronsMaleMiceCCNA2 protein, mouseCyclin A2DNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEzh1 protein, mouseEzh2 protein, mouseHistone-Lysine N-MethyltransferaseNuclear ProteinsPolycomb Repressive Complex 2PRDM2 protein, humanPrdm2 protein, mouseTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID26040698
PMCPMC4513853
OpenAlexW1713502880

What OpenQuestion holds

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LicenceCC BY-NC
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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.