| Project/Area Number |
23657117
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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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 |
IIDA Naoko 国立遺伝学研究所, 生命情報研究センター, 特任研究員 (40360557)
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| Co-Investigator(Renkei-kenkyūsha) |
IIDA Tetsushi 国立遺伝学研究所, 細胞遺伝研究系, 助教 (60391851)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | RNAi / Ago / 細胞周期制御 / Ptr1 / 細胞周期チェックポイント / Ago1 / Arb2化 / タンパク質修飾 |
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| Research Abstract |
RNAi is a conserved mechanism for gene silencing and heterochromatin formation through Argonaute (Ago)-associated complexes. In this study, I focus on a novel role of Ago in the cell-cycle control in S. pombe. Affinity purification of Ago1 revealed novel interaction between Ago1 and Ptr1, an mRNA-export factor. The ptr1-1 mutant impaired the cell cycle arrest but not the silencing. The phenotypic analysis suggested that Ptr1 regulates cell cycle by a distinct mechanism from the RNAi-heterochromatin pathway. I isolated suppressor mutants of ptr1-1 and identified a mutation in TOR-associated gene. I identified the causative mutations by high-throughput sequencing and bioimformatics. This result suggested that Ptr1 and TOR-signaling pathway associated with Ago1.related mechanism
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