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. 2002 Sep 2;158(5):953–965. doi: 10.1083/jcb.200202034

Figure 8.

Figure 8.

N-cadherin–mediated adhesion and myogenesis. N-cadherin activation through cell–cell contact formation affects the RhoA, Rac1, and Cdc42Hs level activation via an unidentified mechanism. The decrease of Rac1 and Cdc42Hs activity leads to a decrease in the JNK level, which allows Myf5 nuclear localization (Meriane et al., 2000) and also favors cell cycle exit (Heller et al., 2001; Meriane et al., 2002). The decreased level of Rac1 and Cdc42Hs activity remains sufficient to allow p38 activity, which is required for MyoD- and MEF-2–responsive genes expression (Zetser et al., 1999; Wu et al., 2000). Elevation of RhoA level activates SRF (Carnac et al., 1998; Wei et al., 1998) and leads to MyoD expression (Gauthier-Rouviere et al., 1996), which allowed p21 and p27-dependent cell cycle exit (Walsh, 1997) and muscle-specific genes expression (Tapscott et al., 1988). RhoA is required for β-catenin localization at the cell–cell contacts sites, another event involved in myogenic induction (Goichberg et al., 2001).