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N-Cadherin-Dependent Cell-Cell Contact Regulates Rho GTPases and β-Catenin Localization in Mouse C2C12 Myoblasts

Sophie Charrasse, Mayya Meriane, Franck Comunale, Anne Blangy and Cécile Gauthier-Rouvière
The Journal of Cell Biology
Vol. 158, No. 5 (Sep. 2, 2002), pp. 953-965
Stable URL: http://www.jstor.org/stable/1621207
Page Count: 13
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N-Cadherin-Dependent Cell-Cell Contact Regulates Rho GTPases and β-Catenin Localization in Mouse C2C12 Myoblasts
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Abstract

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 β-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.

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