Study for the mechanism of N-cadherin endocytosis in synapse

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K18361
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: National Institute for Physiological Sciences
• Principal Investigator: NAGAOKA Tadahiro 生理学研究所, 生体機能調節研究領域, 特別協力研究員 (70634864)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: カドヘリン / 平面内細胞極性因子

Outline of Final Research Achievements

Planar cell polarity protein Vangl2 regulates cell surface expression level of N-cadherin at synapse. To resolve this mechanism is major object of this project. PSD-95 is scaffold protein of post synapse and is shown that complementary localization with N-cadherin in normal neuron. PSD-95 is known as the binding partner of Vangl2 and Vangl2 may responsible for stabilization of PSD-95 localization at the synapse. Because PSD-95 puncta density was decreased and its signal was diffused in dendrite in Vangl2 knockdown neuron. Furthermore, merged localization of PSD-95 and N-cadherin was increased abnormally in Vangl2 knockdown neuron. Therefore we suggested that Vangl2 may regulate proper compartmentalization of PSD-95 and N-cadherin. We also investigate genetic interaction between Vangl2 and N-cadherin and that caused neural tube closure defect.

Free Research Field

分子生物学