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p21(CIP1) and p57(KIP2) control muscle differentiation at the myogenin step

P Zhang1, C Wong, D Liu

  • 1Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030 USA.

Genes & Development
|January 30, 1999
PubMed

Insights

Two cell-cycle inhibitors, p21 and p57, are crucial for muscle cell differentiation. Their combined absence prevents myotube formation, highlighting their essential role in muscle development.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

Background:

  • Cell-cycle arrest is a known prerequisite for muscle cell differentiation.
  • The specific molecules regulating cell-cycle exit and subsequent differentiation remain largely unidentified.

Purpose of the Study:

  • To investigate the roles of Cdk inhibitors p21(CIP1) and p57(KIP2) in skeletal muscle differentiation.
  • To elucidate the relationship between cell-cycle exit and the function of the myogenic transcription factor myogenin.

Main Methods:

  • Utilized a mouse model lacking both p21 and p57 genes.
  • Analyzed myoblast proliferation, apoptosis, and differentiation.
  • Examined myotube formation and endoreplication.
  • Compared developmental defects with those in myogenin-deficient mice.

Main Results:

  • Mice lacking both p21 and p57 exhibit failed myotube formation.
  • These mice show increased myoblast proliferation and apoptosis, along with endoreplication in remaining myotubes.
  • The observed developmental arrest mirrors that of myogenin-deficient mice, suggesting a link between cell-cycle exit and myogenin function.
  • p21, p57, and myogenin expression are coordinately regulated during differentiation.

Conclusions:

  • p21 and p57 redundantly control skeletal muscle differentiation and lung alveoli formation.
  • Cell-cycle exit, regulated by p21 and p57, is essential for myogenin-mediated terminal differentiation.
  • These findings reveal a critical molecular mechanism linking cell-cycle control to muscle development.

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