| Project/Area Number |
15K06945
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Molecular biology
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| Research Institution | Gunma University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
畑田 出穂 群馬大学, 生体調節研究所, 教授 (50212147)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 翻訳停滞解消因子 / ミトコンドリア / リボソーム |
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| Outline of Final Research Achievements |
Mitochondria have two stalled-ribosome rescue factors, ICT1 and C12orf65. Both proteins belong to a family of class I peptide release factors (RFs), all characterized by the presence of a GGQ motif. However, differences of roles in ribosome rescue between ICT1 and C12orf65 remain elusive. Loss of function of the c12orf65 gene causes a mitochondrial translation defect, leading to encephalomyopathy. In this study, we were trying to generate c12orf65 knockout mice by CRISPR/Cas9 technique. We obtained c12orf65-defective heterozygous mice, but we have not obtained any homozygous mice so far. These results suggest embryonic lethality of the homozygous mice. Thus, the functional redundancy between ICT1 and C12orf65 may differ among animals.
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