2017 Fiscal Year Final Research Report
Functional analysis of stalled-ribosome rescue factors in mitochondria
| 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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| Keywords | 翻訳停滞解消因子 / ミトコンドリア |
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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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| Free Research Field |
分子生物学
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