2017 Fiscal Year Annual Research Report

ニューロン樹状突起発達過程のアクチン動態を制御するＭＴＳＳ１の機能解析

Research Project

Project/Area Number	16J11619
Research Institution	Kyoto University
Principal Investigator	川端ケリー京都大学, 生命科学研究科, 特別研究員(DC2)
Project Period (FY)	2016-04-22 – 2018-03-31
Keywords	Purkinje cells / filopodia / MTSS1 / DAAM1 / ARP2/3 / formin / actin / development
Outline of Annual Research Achievements	Using parameters measured from timelapse imaging of MTSS1 knockout Purkinje cells (PCs), I performed a computer simulation to model the effect of increased dendritic protrusion length and observed that the resulting dendritic phenotype was similar to real PCs. I further showed that both MTSS1 and DAAM1 are colocalized at the tips of dendritic protrusions in Purkinje cells. Using TIRF microscopy, I observed that MIM inhibits DAAM1 actin-polymerizing activity, and could also see this negative regulation in cells using SiMS imaging. Induced constitutive active expression of DAAM1 in Purkinje cells resulted in increased filopodia length, similar to our MTSS1 mutant phenotype, suggesting MTSS1 inhibits the activity of DAAM1 in developing dendritic protrusions.
Research Progress Status	29年度が最終年度であるため、記入しない。
Strategy for Future Research Activity	29年度が最終年度であるため、記入しない。