A role of Plexin A2/A4 signaling in layer formation of the mouse cerebral cortex

2016 Fiscal Year Final Research Report

• Project/Area Number: 25430020
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: National Institute for Physiological Sciences
• Principal Investigator: HATANAKA Yumiko 生理学研究所, 基盤神経科学研究領域, 特別協力研究員 (40271548)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 神経発生 / 細胞移動 / 層形成 / 大脳皮質形成 / 細胞間相互作用

Outline of Final Research Achievements

We investigated a phenotype of Plexin A2/A4 double mutant mouse, in which a fraction of upper layer neurons of the cerebral cortex failed to terminate migration and ectopically invaded layer 1. PlexinA2/A4 proteins were expressed on leading processes of upper layer neurons and rescue experiment indicated that Plexin A2/A4 played a cell-autonomous role. On the other hand, Semaphorin 6A, the ligand for Plexin A2/A4, was concentrated in layer 1 and found to originate from radial glial cells in the ventricular zone. These results provide a novel model for termination of neuronal migration; (1) neurons migrate along radial glial cell fiber to reach the top of the cortical plate, (2) Plexin A2/A4-positive leading process touch the distal part of radial glial cell fiber in layer 1, which expresses Semaphorin 6A, and (3) probably due to repulsive effect, interaction between these molecules leads to detachment of migrating neurons from their substrate, thereby terminating migration.

Free Research Field

神経発生学