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First published online 8 April 2008
doi: 10.1242/jcs.020537
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Short Report |
E-catenin is not a significant regulator of β-catenin signaling in the developing mammalian brain
1 Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
2 Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98109, USA
3 Department of Pathology and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98195, USA
* Author for correspondence (e-mail: vvasiouk{at}fhcrc.org)
Accepted 31 January 2008
Summary
β-catenin is a crucial mediator of the canonical Wnt-signaling pathway.
-catenin is a major β-catenin-binding protein, and overexpressed
-catenin can negatively regulate β-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 β-catenin in developing mammalian organisms. We analyzed β-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 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
E-catenin resulted in disruption of intercellular adhesion and hyperplasia in the developing brain, β-catenin signaling was not altered. We conclude that endogenous
E-catenin has no significant impact on β-catenin transcriptional activities in the developing mammalian brain.
Key words: Brain development, β-catenin signaling,
-catenin
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