Premium
αN‐catenin deficiency causes defects in axon migration and nuclear organization in restricted regions of the mouse brain
Author(s) -
Uemura Masato,
Takeichi Masatoshi
Publication year - 2006
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20841
Subject(s) - biology , commissure , axon , morphogenesis , anterior commissure , catenin , axon guidance , population , central nervous system , neuroscience , phenotype , cadherin , nervous system , anatomy , microbiology and biotechnology , cell , gene , genetics , wnt signaling pathway , signal transduction , demography , sociology
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 235:2559–2566, 2006. © 2006 Wiley‐Liss, Inc.