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Related Experiment Videos

Jun inhibits myogenic differentiation.

H Y Su1, T J Bos, F S Monteclaro

  • 1Department of Microbiology, University of Southern California School of Medicine, Los Angeles 90033.

Oncogene
|October 1, 1991
PubMed
Summary
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Avian sarcoma virus 17 (ASV-17) infection inhibits muscle cell differentiation by oncogenic jun gene expression. Transformation-defective Jun proteins, however, are compatible with myogenesis, indicating oncogenic potential is key to inhibition.

Area of Science:

  • Molecular Biology
  • Oncology
  • Developmental Biology

Background:

  • Myogenesis, the process of muscle cell differentiation, is crucial for skeletal muscle development.
  • Oncogenes, such as the jun oncogene, can disrupt normal cellular processes.
  • Avian sarcoma virus 17 (ASV-17) is a retrovirus that carries the jun oncogene.

Purpose of the Study:

  • To investigate the effect of avian sarcoma virus 17 (ASV-17) infection and jun oncogene expression on myoblast differentiation.
  • To determine the relationship between viral jun expression, cellular transformation, and myogenic differentiation.

Main Methods:

  • Infection of chicken and quail myoblasts with ASV-17 and its mutants.
  • Assessment of myoblast fusion, replication, and expression of muscle-specific proteins (desmin, myosin, creatine phosphokinase).

Related Experiment Videos

  • Immunofluorescent staining to detect Gag-Jun fusion protein localization in myoblasts and myotubes.

    • Main Results:

    • High-multiplicity ASV-17 infection inhibited myoblast fusion and muscle-specific protein expression, while promoting replication.
    • Nuclear expression of the ASV-17 Gag-Jun fusion protein was detected in mononuclear myoblasts but not in multinucleated myotubes, suggesting mutual exclusivity.
    • A temperature-sensitive mutant (ts jun-1) with defective transforming ability allowed myotube formation and muscle protein expression, with nuclear Gag-Jun presence, indicating transformation-defective Jun is compatible with myogenesis.
    • Correlation observed between the transforming ability of viral jun constructs and their inhibitory effect on myogenic differentiation.

    Conclusions:

    • Oncogenic expression of the jun gene in myoblasts strongly inhibits myogenic differentiation.
    • Highly transforming Jun proteins are incompatible with the nuclei of differentiating myotubes.
    • Transformation-defective Jun variants can be expressed in the nuclei of differentiating myotubes, supporting myogenesis.