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Vol. 11, Issue 8, 2513-2528, August 2000
*Centre de Recherche de Biochimie Macromoléculaire, Centre
National de la Recherche Scientifique Unité Propre de Recherche
1086, 34293 Montpellier Cedex, France; and The Rho family of GTP-binding proteins plays a critical role in a
variety of cellular processes, including cytoskeletal reorganization and activation of kinases such as p38 and C-jun N-terminal kinase (JNK)
MAPKs. We report here that dominant negative forms of Rac1 and Cdc42Hs
inhibit the expression of the muscle-specific genes myogenin, troponin
T, and myosin heavy chain in L6 and C2 myoblasts. Such inhibition
correlates with decreased p38 activity. Active RhoA, RhoG, Rac1, and
Cdc42Hs also prevent myoblast-to-myotube transition but affect distinct
stages: RhoG, Rac1, and Cdc42Hs inhibit the expression of all
muscle-specific genes analyzed, whereas active RhoA potentiates their
expression but prevents the myoblast fusion process. We further show by
two different approaches that the inhibitory effects of active Rac1 and
Cdc42Hs are independent of their morphogenic activities. Rather,
myogenesis inhibition is mediated by the JNK pathway, which also leads
to a cytoplasmic redistribution of Myf5. We propose that although Rho
proteins are required for the commitment of myogenesis, they differentially influence this process, positively for RhoA and Rac1/Cdc42Hs through the activation of the SRF and p38 pathways, respectively, and negatively for Rac1/Cdc42Hs through the activation of
the JNK pathway.
Institut de
Génétique Humaine, Centre National de la Recherche
Scientifique Unité Propre de Recherche 1142, 34396 Montpellier
Cedex 5, France
Corresponding author. E-mail address:
gauthier{at}crbm.cnrs-mop.fr.
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