Investigation of a physiological role of endosome-mitochondrial interaction by fluorescence bioimaging

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K15023
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General physiology
• Research Institution: Hokkaido University
• Principal Investigator: Ohba Yusuke 北海道大学, 医学(系)研究科(研究院), 教授 (30333503)
• Co-Investigator(Renkei-kenkyūsha): Nanbo Asuka 北海道大学, 大学院医学研究院, 准教授 (60359487) ; Nishide Shinya 北海道大学, 大学院医学研究院, 助教 (40451398) ; Fujioka Yoichiro 北海道大学, 大学院医学研究院, 助教 (70597492)
• Research Collaborator: Fujioka Mari ; Horiuchi Kosui ; Satoh Aya O.
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 細胞内小器官 / シグナル伝達 / エンドサイトーシス / ミトコンドリア

Outline of Final Research Achievements

We have reported that the complex of small G protein Ras and its target molecule PI3K is localized in the endosomes and controls endocytosis and viral particle internalization. However, the molecular mechanism by which the Ras-PI3K complex is localized is the endosome remains unknown. In this study, the amino acid sequence responsible for the above phenomenon was identified. By screening the binding protein for the sequence, a mitochondrial protein was identified. Knockdown of this mitochondrial protein inhibited the translocation of Ras-PI3K complex to the endosome, endocytosis, and mitochondrial-endosome interaction, suggesting that binding of PI3K and the factor regulates endocytosis through interaction between organelles.

Free Research Field

細胞生理学