| Project/Area Number |
16K18495
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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 |
Molecular biology
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| Research Institution | National Institute of Genetics |
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Principal Investigator |
Shiratsuchi Gen 国立遺伝学研究所, 分子遺伝研究系, 特任研究員 (80625533)
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| Research Collaborator |
KITAGAWA Daiju 国立遺伝学研究所, 分子遺伝研究系, 教授 (80605725)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | non-coding RNA / noncoding RNA / 核酸 / 細胞生物学 / 分子生物学 / 細胞分裂 |
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| Outline of Final Research Achievements |
Although long non-coding RNAs (lncRNAs) have been revealed to function in a wide range of biological phenomena, the lncRNAs that function in specific mitotic events are poorly understood yet. In this study, I characterized a novel human lncRNA, named CENNA1 (Centrosomal Non-coding RNA 1) that had been identified as a novel regulator of mitosis by our group. I found that depletion of CENNA1 significantly impaired the establishment of kinetochore-microtubule attachment, accompanied with the loss of CLIP170, a member of conserved microtubule plus-end tracking proteins, from the kinetochores. This study sheds light on the new aspect of lncRNA that controls chromosome segregation and would provide a new avenue to the future cell division research.
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