Abstract
Myogenesis is a complex process characterized by both biochemical and morphological differentiation. Recent transfection studies suggested a close relationship between the GLUT 3 transporter and the myogenic ability of rat skeletal L6 myoblast. In this study, the myogenic properties of GLUT 3 − mutants were examined. Studies using three different GLUT 3 − mutants (D2, D9 and D23) revealed that these mutants were defective not only in the GLUT 3 transporter, but also in the expression of myogenesis-associated genes. The properties of mutant D23 were further characterized. Overexpression of an exogenous functional GLUT 3 transporter was unable to restore the myogenic defects of this mutant. This mutant was subsequently found to be altered in components acting on at least two different sites of the L6 myogenic pathway. Transfection studies revealed that mutant D23 was deficient in component(s) essential for the myogenin promoter activity. The second component was required for the transcription of muscle-specific protein genes, as overexpression of myogenin was unable to rescue the inability of this mutant to express muscle-specific genes and to form myotubes. Mutant D23 was therefore thought to be deficient in a regulatory component which controlled the expression of GLUT 3, myogenin and muscle-specific genes.
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