The regulation of mitochondrial quality by cytoskeleton molecules

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K21055
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General anatomy (including histology/embryology); Pathological medical chemistry
• Research Institution: Hamamatsu University School of Medicine
• Principal Investigator: KONDO Takeshi 浜松医科大学, 医学部, 特任助教 (10712705)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 細胞骨格 / ミトコンドリア / パーキンソニズム

Outline of Final Research Achievements

In this study, we aimed to clarify the roles of γ-tubulin proteins in the regulation of mitochondrial quality and the molecular mechanisms of neurodegenerative diseases. Through analyzing Tubg2-KO mice, we found that TUBG2 protein functions not only in the microtubule nucleation, but also in the quality control of mitochondria. Moreover, γ-tubulin proteins are decreased in some of human neurodegenerative diseases with parkinsonism. These findings indicate that loss of TUBG2 could lead to exaggeration of these diseases by defects in mitochondria.

Free Research Field

細胞生物学