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J Cell Sci. 2008 May 1;121(Pt 9):1357-62. doi: 10.1242/jcs.020537. Epub 2008 Apr 8.

alphaE-catenin is not a significant regulator of beta-catenin signaling in the developing mammalian brain.

Author information

1
Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.

Abstract

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

PMID:
18397997
PMCID:
PMC2586592
DOI:
10.1242/jcs.020537
[Indexed for MEDLINE]
Free PMC Article

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