Fig. 9. mDiaN3 controls MyoD by reciprocal regulation of two transcription factors. A model for dual signaling to the MyoD gene by mDia via positive regulation of a directly acting Rho-actin-SRF pathway and negative regulation of an indirect APC–-catenin–TCF pathway. Actin assembly factors bind to the FH1 and FH2 domains, drive polymerization of microfilaments to activate SRF via MAL release and thereby induce MyoD expression. The interaction of mDia with APC may increase cytoplasmic degradation of -catenin or reduce nuclear shuttling of APC and thereby promote cytoplasmic retention of -catenin. As dnTCF inhibits MyoD, TCF may play an activating role by inducing positive upstream factors (X). Taken together, the data suggest that MyoD expression is suppressed by any perturbation of mDia, because SRF and TCF are reciprocally regulated by this key signaling adaptor protein.