Evidence map›Paper›PMID 25271443›Full record

ArticlePloS one2014

The SWI/SNF subunit/tumor suppressor BAF47/INI1 is essential in cell cycle arrest upon skeletal muscle terminal differentiation.

Véronique Joliot, Ouardia Ait-Mohamed, Valentine Battisti, Julien Pontis, Ophélie Philipot, Philippe Robin, Hidenori Ito, Slimane Ait-Si-Ali

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025
    Review
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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

8 authors.

Véronique JoliotUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.
Ouardia Ait-MohamedUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.
Valentine BattistiUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.
Julien PontisUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.
Ophélie PhilipotUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.
Philippe RobinUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.
Hidenori ItoDepartment of Molecular Neurobiology, Institute for Developmental Research, Aichi Human Service Center, Aichi, Japan.
Slimane Ait-Si-AliUniversité Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myogenic terminal differentiation is a well-orchestrated process starting with permanent cell cycle exit followed by muscle-specific genetic program activation. Individual SWI/SNF components have been involved in muscle differentiation. Here, we show that the master myogenic differentiation factor MyoD interacts with more than one SWI/SNF subunit, including the catalytic subunit BRG1, BAF53a and the tumor suppressor BAF47/INI1. Downregulation of each of these SWI/SNF subunits inhibits skeletal muscle terminal differentiation but, interestingly, at different differentiation steps and extents. BAF53a downregulation inhibits myotube formation but not the expression of early muscle-specific genes. BRG1 or BAF47 downregulation disrupt both proliferation and differentiation genetic programs expression. Interestingly, BRG1 and BAF47 are part of the SWI/SNF remodeling complex as well as the N-CoR-1 repressor complex in proliferating myoblasts. However, our data show that, upon myogenic differentiation, BAF47 shifts in favor of N-CoR-1 complex. Finally, BRG1 and BAF47 are well-known tumor suppressors but, strikingly, only BAF47 seems essential in the myoblasts irreversible cell cycle exit. Together, our data unravel differential roles for SWI/SNF subunits in muscle differentiation, with BAF47 playing a dual role both in the permanent cell cycle exit and in the regulation of muscle-specific genes.

Indexed as

Cell Cycle CheckpointsCell DifferentiationChromosomal Proteins, Non-HistoneDNA-Binding ProteinsHeLa CellsHumansMuscle DevelopmentMuscle, SkeletalMyoD ProteinSMARCB1 ProteinTranscription FactorsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsMyoD ProteinSMARCB1 ProteinSMARCB1 protein, humanTranscription Factors

Identifiers

PMID25271443
PMCPMC4182762

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Registered trials

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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.