First published online April 23, 2008
Journal of Cell Science 121, 904e (2008)
© The Company of Biologists Limited
E-catenin bows out
The protein β-catenin is involved in intercellular adhesion and in the regulation of the canonical Wnt signalling pathway; it is also known to have an important role in regulating the proliferation of embryonic neural progenitor cells. 
-catenin is a major binding partner of β-catenin and studies that have used the overexpression or knockdown of -catenin in cultured cell lines have indicated a role for -catenin as a negative regulator of the transcriptional activity of β-catenin. Here, Vasioukhin and colleagues (p. 1357) use a loss-of-function approach to analyze whether depletion of the major epithelial -catenin, E-catenin, results in changes in the transcriptional activity of β-catenin in the developing brain. The authors previously showed that mice with a conditional deletion of E-catenin in the central nervous system display massive brain hyperplasia and dysplasia; in this report, they hypothesize that the deletion of E-catenin activates β-catenin, which might be at least partially responsible for the hyperplasia. They find that loss of E-catenin results in the disruption of intercellular adhesion and hyperplasia in the developing mouse brain but, surprisingly, the β-catenin signalling pathway is not altered. These results suggest that -catenin has no significant impact on β-catenin signalling in vivo.
Related articles in JCS:
- E-catenin is not a significant regulator of β-catenin signaling in the developing mammalian brain
- Wen-Hui Lien, Olga Klezovitch, Manda Null, and Valeri Vasioukhin
JCS 2008 121: 1357-1362.
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