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RhoA GTPase and serum response factor control selectively the expression of MyoD without affecting Myf5 in mouse
G Carnac1, M Primig, M Kitzmann
1Cell Biology Unit, IGH, Centre National de la Recherche Scientifique, UPR 1142, 34396 Montpellier cédex 5, France.
Molecular Biology of the Cell
|July 11, 1998
Summary
MyoD gene expression requires RhoA and serum response factor (SRF), while Myf5 does not. This study reveals distinct regulatory pathways for these key skeletal muscle differentiation factors.
Area of Science:
- Molecular Biology
- Cell Biology
- Developmental Biology
Background:
- MyoD and Myf5 are basic helix-loop-helix transcription factors crucial for skeletal muscle differentiation.
- Their precise regulation during development and in response to stimuli is not fully understood.
- Serum response factor (SRF) is known to regulate MyoD expression.
Purpose of the Study:
- To investigate if SRF regulates Myf5 gene expression.
- To explore the role of Rho family G-proteins (RhoA, Rac, CDC42) in regulating MyoD and Myf5.
- To elucidate the signaling pathways controlling MyoD and Myf5 expression.
Main Methods:
- Gene expression analysis in C2 muscle cells.
- Inactivation of SRF.
- Inhibition of Rho family G-proteins using lovastatin, C3-transferase, and dominant-negative RhoA.
- Analysis of MyoD and Myf5 protein levels and promoter activity.
Main Results:
- SRF inactivation rapidly extinguished MyoD expression but did not affect Myf5 expression.
- RhoA, but not Rac or CDC42, was essential for MyoD expression.
- Inhibition of RhoA activity significantly decreased MyoD protein levels and promoter activity, without impacting Myf5.
- RhoA-dependent activation of MyoD transcription required functional SRF.
Conclusions:
- MyoD and Myf5 are regulated by distinct upstream pathways.
- MyoD expression is specifically controlled by a RhoA/SRF signaling cascade.
- This study establishes a link between RhoA activity and the regulation of a key muscle regulator, MyoD.
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