2021 Fiscal Year Final Research Report
Cooperative regulation of cytoskeleton and membrane dynamics by novel mechanism of dynamin
Project/Area Number |
19H03225
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Review Section |
Basic Section 44010:Cell biology-related
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Research Institution | Okayama University |
Principal Investigator |
Takei Kohji 岡山大学, 医歯薬学域, 教授 (40322226)
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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)
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Project Period (FY) |
2019-04-01 – 2022-03-31
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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.
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Free Research Field |
細胞生物学
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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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