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MASTR directs MyoD-dependent satellite cell differentiation during skeletal muscle regeneration.

In response to skeletal muscle injury, satellite cells, which function as a myogenic stem cell population, become activated, expand through proliferation, and ultimately fuse with each other and with damaged myofibers to promote muscle regeneration. Here, we show that members of the Myocardin family of transcriptional coactivators, MASTR and MRTF-A, are up-regulated in satellite cells in response to skeletal muscle injury and muscular dystrophy. Global and satellite cell-specific deletion of MASTR in mice impairs skeletal muscle regeneration. This impairment is substantially greater when MRTF-A is also deleted and is due to aberrant differentiation and excessive proliferation of satellite cells. These abnormalities mimic those associated with genetic deletion of MyoD, a master regulator of myogenesis, which is down-regulated in the absence of MASTR and MRTF-A. Consistent with an essential role of MASTR in transcriptional regulation of MyoD expression, MASTR activates a muscle-specific postnatal MyoD enhancer through associations with MEF2 and members of the Myocardin family. Our results provide new insights into the genetic circuitry of muscle regeneration and identify MASTR as a central regulator of this process.

Pubmed ID: 22279050


  • Mokalled MH
  • Johnson AN
  • Creemers EE
  • Olson EN


Genes & development

Publication Data

January 15, 2012

Associated Grants

  • Agency: NHLBI NIH HHS, Id: R01 HL093039

Mesh Terms

  • Animals
  • Cell Differentiation
  • Cell Proliferation
  • Cells, Cultured
  • Enhancer Elements, Genetic
  • Female
  • Gene Deletion
  • Gene Expression Profiling
  • Gene Expression Regulation, Developmental
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Muscle Development
  • Muscle, Skeletal
  • MyoD Protein
  • Myogenic Regulatory Factors
  • Protein Binding
  • Regeneration
  • Satellite Cells, Skeletal Muscle
  • Trans-Activators