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. 2018 Nov 20;11:422. doi: 10.3389/fnmol.2018.00422

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Copyright © 2018 Chen, Lu and Tsai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed model for Cntn1 function in the neuronal migration during corticogenesis (A) In the normal brain, newborn neurons (blue) migrate from the VZ along the radial fiber of RGCs to the CP (Kriegstein and Noctor, 2004). Cntn1 dysfunction arrests neurons in the multipolar stage and caused branching of the leading process in the bipolar stage. These phenotypes lead to defects in neuronal migration. These defects can be rescued by inhibition of RhoA activities. (B) At the molecular level, our results suggest that Cntn1 regulates neurite morphologies and neuronal migration through inhibiting RhoA activity during cortical development. Loss of Cntn1 increases RhoA activity causing neuronal migration defects.