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Cyclins and cyclin-dependent kinases are differentially regulated during terminal differentiation of C2C12 muscle

L Jahn1, J Sadoshima, S Izumo

  • 1Molecular Medicine Division, Beth Israel Hospital, Boston, Massachusetts.

Experimental Cell Research
|June 1, 1994
PubMed

Insights

Skeletal muscle differentiation involves cell cycle gene regulation. Key cell cycle proteins like cdc2 and cyclins are downregulated, preventing re-entry into the cell cycle and maintaining the postmitotic state.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Developmental Biology

Background:

  • Skeletal myogenesis involves terminal differentiation and cell cycle exit.
  • Understanding cell cycle gene regulation during muscle differentiation is crucial.

Purpose of the Study:

  • Investigate cell cycle gene expression, activity, and localization during C2C12 myogenesis.
  • Determine the role of cyclins and cyclin-dependent kinases in terminal differentiation.

Main Methods:

  • Utilized the mouse skeletal myogenic cell line C2C12.
  • Monitored mRNA and protein levels of cyclins and cyclin-dependent kinases (cdks).
  • Assessed histone H1 kinase activity and protein localization via serum deprivation and restimulation.

Main Results:

  • cdc2 mRNA and p34cdc2 protein decreased during differentiation but were reinduced by serum.
  • Cyclin A, B, and C mRNA levels were downregulated.
  • Cyclin D1 mRNA transiently increased, while cyclin D3 remained constant.
  • p34cdc2 protein was absent in mature myotubes, and its kinase activity decreased.
  • p33cdk2 levels and activity remained unchanged.

Conclusions:

  • Terminal skeletal muscle differentiation involves differential regulation of cyclins and cdks.
  • The inability of differentiated myotubes to accumulate p34cdc2 protein may maintain the postmitotic state.
  • This regulation is critical for muscle cell permanence, even with growth factor presence.

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