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Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
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The SWI/SNF subunit/tumor suppressor BAF47/INI1 is essential in cell cycle arrest upon skeletal muscle terminal

Véronique Joliot1, Ouardia Ait-Mohamed1, Valentine Battisti1

  • 1Université Paris Diderot, Sorbonne Paris Cité, Centre Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot, Paris, France.

Plos One
|October 2, 2014
PubMed

Insights

The SWI/SNF complex subunits BRG1 and BAF47 are crucial for skeletal muscle differentiation and cell cycle exit. BAF47 plays a dual role in cell cycle exit and muscle gene regulation.

Area of Science:

  • Muscle biology
  • Cellular differentiation
  • Epigenetics

Background:

  • Myogenic terminal differentiation involves cell cycle exit and muscle gene activation.
  • SWI/SNF complex components are implicated in muscle differentiation.

Purpose of the Study:

  • To investigate the roles of SWI/SNF subunits (BRG1, BAF53a, BAF47) in myogenic terminal differentiation.
  • To elucidate the interaction of MyoD with SWI/SNF subunits and their functions in muscle development.

Main Methods:

  • Investigated the interaction between MyoD and SWI/SNF subunits.
  • Analyzed the effects of downregulating SWI/SNF subunits on skeletal muscle differentiation.
  • Examined the composition of SWI/SNF and N-CoR-1 complexes during myogenesis.

Main Results:

  • Downregulation of BRG1, BAF53a, or BAF47 differentially inhibited skeletal muscle terminal differentiation.
  • BAF53a downregulation affected myotube formation but not early gene expression.
  • BRG1 and BAF47 downregulation disrupted both proliferation and differentiation gene programs.
  • BAF47 shifted to the N-CoR-1 complex during differentiation.
  • BAF47, but not BRG1, was essential for irreversible cell cycle exit in myoblasts.

Conclusions:

  • SWI/SNF subunits exhibit differential roles in muscle differentiation.
  • BAF47 plays a critical dual role in permanent cell cycle exit and muscle-specific gene regulation.

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