E-catenin is not a significant regulator of -catenin signaling in the developing mammalian brain

-catenin is a crucial mediator of the canonical Wnt-signaling pathway. -catenin is a major -catenin-binding protein, and overexpressed -catenin can negatively regulate -catenin activity. Thus, -catenin may be an important modulator of the Wnt pathway. We show here that endogenous -catenin has little impact on the transcriptional activity of -catenin in developing mammalian organisms. We analyzed -catenin signaling in mice with conditional deletion of E-catenin (Ctnna1) in the developing central nervous system. This mutation results in brain hyperplasia and we investigated whether activation of -catenin signaling may be at least partially responsible for this phenotype. To reveal potential quantitative or spatial changes in -catenin signaling, we used mice carrying a -catenin-signaling reporter transgene. In addition, we analyzed the expression of known endogenous targets of the -catenin pathway and the amount and localization of -catenin in mutant progenitor cells. We found that although loss of E-catenin resulted in disruption of intercellular adhesion and hyperplasia in the developing brain, -catenin signaling was not altered. We conclude that endogenous E-catenin has no significant impact on -catenin transcriptional activities in the developing mammalian brain.