| Project/Area Number |
18H02375
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 43010:Molecular biology-related
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| Research Institution | Osaka University |
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Principal Investigator |
Kai Toshie 大阪大学, 生命機能研究科, 教授 (40579786)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2020: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2018: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
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| Keywords | piRNA / Drosophila meganogaster / germline / 生殖細胞 / トランスポゾン / Tudor domain / ピンポン増幅 |
|---|
| Outline of Final Research Achievements |
In this research project, we analyzed the functions of Tudor domain proteinss (Tdrd) that function in the biogenesis of a class of gonad specific small RNAs, called piRNA, those suppress transposons. In tdrd1 mutant testes, piRNA biogenesis was affected, causing upregulation of Stellate protein. As expected, Tdrd1 protein physically interacted with Piwi family proteins. In addition, it turned out that Drosophila Tdrd9, an RNA helicase containing functioning in piRNA pathway, translocated to the cytoplasm depending on the intrinsically disordered region of other Tdrd proteins, and forms a piRNA processing complex different from that with the other RNA helicase, Vasa.
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| Academic Significance and Societal Importance of the Research Achievements |
トランスポゾンを抑制し、生殖細胞のゲノムを保護するpiRNAの生合成に関わるTudorドメインタンパク質（Tdrd）群の機能解析を行い、ショウジョウバエTdrd1の機能を明らかにした。またTdrd9が核から細胞質へ移行する機構の一端も明らかにした。これらの機能が破綻すると、ゲノムが不安定になり、生殖細胞の発生が損なわれ、動物は不妊となる。
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