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2021 Fiscal Year Final Research Report

Cooperative regulation of cytoskeleton and membrane dynamics by novel mechanism of dynamin

Research Project

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Project/Area Number 19H03225
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Review Section Basic Section 44010:Cell biology-related
Research InstitutionOkayama University

Principal Investigator

Takei Kohji  岡山大学, 医歯薬学域, 教授 (40322226)

Co-Investigator(Kenkyū-buntansha) 山田 浩司  岡山大学, 医歯薬学域, 准教授 (80325092)
竹田 哲也  岡山大学, 医歯薬学域, 研究准教授 (30302368)
内橋 貴之  名古屋大学, 理学研究科, 教授 (30326300)
Project Period (FY) 2019-04-01 – 2022-03-31
Keywordsダイナミン / アクチン / 微小管 / 細胞膜
Outline of Final Research Achievements

We found that Charcot-Marie-Tooth disease-associated mutations of dynamin 2 cause aberrant stress fibers, showing that dynamin is required for the formation and stabilization of stress fibers. And we reconstituted in vitro the actin bundle formation by dynamin. We also found that dynamin 1 bundles microtubules, and showed that this bundling is necessary for the primary processes formation and stabilization of cell morphology of renal glomerular podocytes. The microtubule-binding site of dynamin 1 was identified. Furthermore, regarding the regulation of membrane dynamics, we demonstrated that dynamin 2 and BIN1, a BAR protein, cooperatively function in T-tubule formation and stabilization of skeletal muscle cells.

Free Research Field

細胞生物学

Academic Significance and Societal Importance of the Research Achievements

ダイナミンの変異が、てんかん性脳症や末梢神経変性疾患Charcot-Marie-Tooth病、先天性筋疾患の一つである中心核ミオパチーの原因となることがわかり、それらの疾患に関連するダイナミン変異も多数報告されている。ダイナミン分子の生理的機能、作動機構を解明するとともに、変異に伴う機能破綻のメカニズムを明らかにすることは、これらの難治性疾患の分子病態の解明や新規の診断、治療の開発に不可欠である。

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Published: 2023-01-30  

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