Molecular analyses of crossing-proof mechanism of dendrites

2014 Fiscal Year Final Research Report

• Project/Area Number: 24500410
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: Kyoto University
• Principal Investigator: USUI Tadao 京都大学, 生命科学研究科, 助教 (10324708)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 樹状突起 / 突起間交差忌避 / 細胞間認識タンパク質

Outline of Final Research Achievements

Our research group has clarified the essential signaling mechanism of the normal extension of dendrites in the Drosophila model system. We have showed that both seven-transmembrane cadherin molecules Flamingo and intracellular binding molecule Espinas prevented cooperatively the dendrites from crossing with each other. By using RNA interference method and Cas9/CRISPR method, we found that intracellular scaffold protein Neurochondrin, one of the identified group of molecules as Espinas binding factor, displayed a similar crossing defects as that of Espinas mutant.

Free Research Field

神経科学