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αN-catenin deficiency causes defects in axon migration and nuclear organization in restricted regions of the mouse brain
Article first published online: 9 AUG 2006
DOI: 10.1002/dvdy.20932
Copyright © 2006 Wiley-Liss, Inc.
Issue
Developmental Dynamics
Special Issue: Mouse Development Special Issue
Volume 235, Issue 9, page spc1, September 2006
Additional Information
How to Cite
Uemura, M. and Takeichi, M. (2006), αN-catenin deficiency causes defects in axon migration and nuclear organization in restricted regions of the mouse brain. Dev. Dyn., 235: spc1. doi: 10.1002/dvdy.20932
Publication History
- Issue published online: 9 AUG 2006
- Article first published online: 9 AUG 2006
Funded by
- Specially Promoted Research of the Ministry of Education, Science, Sports, and Culture of Japan
- Abstract
- Cited By
Keywords:
- anterior commissure;
- cadherin;
- catenin;
- inferior olive;
- mammillary body
Abstract
αN-catenin is a cadherin-binding protein, widely expressed in the nervous system; and it plays a crucial role in cadherin-mediated cell-cell adhesion. Here we report the effects of αN-catenin gene deficiency on brain morphogenesis. In addition to the previously reported phenotypes, we found that some of the axon tracts did not normally develop, in particular, axons of the anterior commissure failed to cross the midline, migrating, rather, to ectopic places. In restricted nuclei, a population of neurons was missing or their laminar arrangement was distorted. The ventricular structures were also deformed. These results indicate that αN-catenin has diverse roles in the organization of the central nervous system, but only in limited portions of the brain. Developmental Dynamics, 2006. © 2006 Wiley-Liss, Inc.