| Project/Area Number |
15K18501
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional biochemistry
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| Research Institution | Niigata University |
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Principal Investigator |
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| Research Collaborator |
JIN Xiulian
MIHARA Katsuyoshi
OTERA Hidenori
YAMASHITA Tomohiro
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | マイトファジー / オートファジー / ミトコンドリア / Drp1 / ミトコンドリア分裂 / オートファゴソーム |
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| Outline of Final Research Achievements |
Mitochondria produce the vast majority of cellular energy and are essential organelles for cell survival. A damaged portion of mitochondria is degraded by autophagy (termed mitophagy) and mitophagy contributes to mitochondrial homeostasis. It has been believed so far that mitochondrial division occurs first and then the divided mitochondrial portion is recognized by autopahgy. However, morphological properties of mitochondria during mitophagy remain unclear. In the present study, I have discovered a novel division pathway of mitochondria during mitophagy. In the course of this pathway, first, mitochondrial portion of tubular mitochondria is recognized by isolation membrane. And then, the portion buds simultaneously with isolation membrane elongation. Finally, the mitochondrial portion is separated from tubular mitochondria and is completely enwrapped by autophagosome.
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