| Project/Area Number |
17K19645
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine and related fields
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Tanaka Yosuke 東京大学, 医科学研究所, 助教 (10509087)
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
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| Keywords | 造血幹細胞 / 非対称分裂 / midbody / Midbody / 対称・非対称分裂 |
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| Outline of Final Research Achievements |
The aim of this project is to reveal relationships between asymmetric cell division of hematopoietic stem cells(HSCs) and asymmetric distribution of Midbody. We planed to generate a midbody reporter mouse line using fusion protein between MgcRacGAP(MRG; a midbody marker) and hmKuO2, but it is still ongoing. We also examined relationships between maintenance of multipoetncy of HSCs and asymmetric distribution of midbody in vitro using HSCs retrovirally transduced with MRG-hmKuO2 and found that daughter cells that released midbody tended to maintain their multipotency after cell divisions.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の肝であったレポーターマウスの作製が難航し研究目標達成には至らなったが、レトロウイルスベクターによりmidbodyマーカーを導入した造血幹細胞を用いた研究において、①細胞分裂におけるmidbodyの継承は細胞の分化運命に影響を与えること、②midbodyを継承した娘細胞はmidbodyを継承しなかった娘細胞と比べて細胞分裂・分化が抑制されることを明らかにした。今回の結果は、細胞分裂におけるmidbodyの継承の有無がその後の細胞の分化運命に影響を与えることを初めて実験的に示したもでのであり、学術的意義は大きい。
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