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Vol. 9, Issue 7, 1891-1902, July 1998
*Cell Biology Unit, IGH, Centre National de la Recherche
Scientifique, UPR 1142, 34396 Montpellier cédex 5, France;
MyoD and Myf5 belong to the family of basic helix-loop-helix
transcription factors that are key operators in skeletal muscle differentiation. MyoD and Myf5 genes are selectively activated during
development in a time and region-specific manner and in response to
different stimuli. However, molecules that specifically regulate the
expression of these two genes and the pathways involved remain to be
determined. We have recently shown that the serum response factor
(SRF), a transcription factor involved in activation of both mitogenic
response and muscle differentiation, is required for MyoD gene
expression. We have investigated here whether SRF is also involved in
the control of Myf5 gene expression, and the potential role of upstream
regulators of SRF activity, the Rho family G-proteins including Rho,
Rac, and CDC42, in the regulation of MyoD and Myf5. We show that
inactivation of SRF does not alter Myf5 gene expression, whereas it
causes a rapid extinction of MyoD gene expression. Furthermore, we show
that RhoA, but not Rac or CDC42, is also required for the expression of
MyoD. Indeed, blocking the activity of G-proteins using the general
inhibitor lovastatin, or more specific antagonists of Rho proteins such as C3-transferase or dominant negative RhoA protein, resulted in a
dramatic decrease of MyoD protein levels and promoter activity without
any effects on Myf5 expression. We further show that RhoA-dependent transcriptional activation required functional SRF in C2 muscle cells.
These data illustrate that MyoD and Myf5 are regulated by different
upstream activation pathways in which MyoD expression is specifically
modulated by a RhoA/SRF signaling cascade. In addition, our results
establish the first link between RhoA protein activity and the
expression of a key muscle regulator.
Institut Pasteur,
Molecular Biology of the Cell
Vol. 9, 1891-1902, July 1998
Copyright © 1998 by The American Society for Cell Biology
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