Alpha N-catenin deficiency causes defects in axon migration and nuclear organization in restricted regions of the mouse brain

Dev Dyn. 2006 Sep;235(9):2559-66. doi: 10.1002/dvdy.20841.

Abstract

Alpha N-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 alpha N-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 alpha N-catenin has diverse roles in the organization of the central nervous system, but only in limited portions of the brain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / metabolism
  • Axons / ultrastructure
  • Brain / embryology*
  • Brain / metabolism*
  • Cell Movement
  • Female
  • Gene Expression Regulation, Developmental
  • In Situ Hybridization
  • Mammillary Bodies / embryology
  • Mammillary Bodies / metabolism
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins / deficiency*
  • Nerve Tissue Proteins / genetics
  • Olivary Nucleus / embryology
  • Olivary Nucleus / metabolism
  • Pregnancy
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Septal Nuclei / embryology
  • Septal Nuclei / metabolism
  • alpha Catenin / deficiency*
  • alpha Catenin / genetics

Substances

  • Ctnna2 protein, mouse
  • Nerve Tissue Proteins
  • RNA, Messenger
  • alpha Catenin