• H-T Wang, L Zeng, Q Chen, X Zhang, J-W Liu, T-J Lu, Z-Q Xiong, J Zheng, and Z-L Hu.
• Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237, China.
• Neuroscience. 2015 Jan 22;284:273-82.

AbstractIn mice, the compact hippocampal primordium is formed during the prenatal stage by early-generated neurons that migrate from the lateral ventricular zone. However, despite much being understood about the formation of the hippocampus, the molecular mechanisms that maintain the morphology of the hippocampal primordium after its formation remain to be characterized. β-Catenin is a key factor of canonical Wnt signaling and also a component of adherens junctions. Previous embryonic deletion studies have demonstrated that β-catenin is required for early development and generation of granule cells. However, whether β-catenin is involved in the morphological maintenance of the hippocampus as a cell adhesion molecule is still unknown. Here, we report that perinatal deletion of β-catenin in postmitotic neurons and some radial glial cells of hippocampus using CamKIIα-iCre; β-cateninflox/flox conditional knockout mice, leads to disorganization of the radial glial scaffold and consequentially severe defects in hippocampal morphology. We demonstrate that β-catenin is required for maintaining radial glial scaffold possibly via its well-known role in cell adhesion during the perinatal period. These findings provide essential advances into our understanding of the maintenance of the hippocampal primordium during the perinatal period.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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