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Published 3 September 2002. doi:10.1083/jcb.200202034
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© The Rockefeller University Press, 0021-9525/2002/9/953 $5.00
The Journal of Cell Biology, Volume 158, Number 5, September 2, 2002 953-965

Article

N-cadherin–dependent cell–cell contact regulates Rho GTPases and ß-catenin localization in mouse C2C12 myoblasts



Sophie Charrasse, Mayya Meriane, Franck Comunale, Anne Blangy and Cécile Gauthier-Rouvière

Centre de Recherche de Biochimie Macromoléculaire, 34293 Montpellier Cedex, France

Address correspondence to Cécile Gauthier-Rouvière, Centre de Recherche de Biochimie Macromoléculaire (CRBM), CNRS UPR 1086, 1919 Route de Mende, 34293 Montpellier Cedex, France. Tel.: 33-4-6761-3355. Fax: 33-4-6752-1559. E-mail: gauthier{at}crbm.cnrs-mop.fr

N-cadherin, a member of the Ca2+-dependent cell–cell adhesion molecule family, plays an essential role in skeletal muscle cell differentiation. We show that inhibition of N-cadherin–dependent adhesion impairs the upregulation of the two cyclin-dependent kinase inhibitors p21 and p27, the expression of the muscle-specific genes myogenin and troponin T, and C2C12 myoblast fusion. To determine the nature of N-cadherin–mediated signals involved in myogenesis, we investigated whether N-cadherin–dependent adhesion regulates the activity of Rac1, Cdc42Hs, and RhoA. N-cadherin–dependent adhesion decreases Rac1 and Cdc42Hs activity, and as a consequence, c-jun NH2-terminal kinase (JNK) MAPK activity but not that of the p38 MAPK pathway. On the other hand, N-cadherin–mediated adhesion increases RhoA activity and activates three skeletal muscle-specific promoters. Furthermore, RhoA activity is required for ß-catenin accumulation at cell–cell contact sites. We propose that cell–cell contacts formed via N-cadherin trigger signaling events that promote the commitment to myogenesis through the positive regulation of RhoA and negative regulation of Rac1, Cdc42Hs, and JNK activities.

Key Words: N-cadherin; Rho GTPases; JNK; ß-catenin, myogenesis; PL, polylysine


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