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

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