Key result
Analysis of mice with targeted null mutations reveals that MyoD or Myf-5 is sufficient for skeletal myoblast formation, while myogenin is essential for terminal differentiation of myotubes.
The review highlights the functional redundancy of MyoD and Myf-5 in skeletal myoblast formation and the distinct, essential role of myogenin in terminal differentiation.
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Establishes foundational myogenic roles in skeletal muscle; leaves open extension to cardiac regeneration or human applications.
Gene targeting has allowed the dissection of complex biological processes at the genetic level. Our understanding of the nuances of skeletal muscle development has been greatly increased by the analysis of mice carrying targeted null mutations in the Myf-5, MyoD and myogenin genes, encoding members of the myogenic regulatory factor (MRF) family. These experiments have elucidated the hierarchical relationships existing between the MRFs, and established that functional redundancy is a feature of the MRF regulatory network. Either MyoD or Myf-5 is sufficient for the formation or survival of skeletal myoblasts. Myogenin acts later in development and plays an essential in vivo role in the terminal differentiation of myotubes.
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Rudnicki et al. (1995) conducted a review in Skeletal muscle development. Targeted null mutations in Myf-5, MyoD and myogenin genes was evaluated. Analysis of mice with targeted null mutations reveals that MyoD or Myf-5 is sufficient for skeletal myoblast formation, while myogenin is essential for terminal differentiation of myotubes.
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