The regulation of mitochondrial quality by cytoskeleton molecules

• 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
• Project Status: Completed (Fiscal Year 2017)
• Budget Amount: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000); Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000); Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
• Keywords: 細胞骨格 / ミトコンドリア / パーキンソニズム / 神経変性疾患 / パーキソニズム

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.