| Project/Area Number |
16H07422
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Molecular biology
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| Research Institution | Tokyo Institute of Technology (2017)
National Institute for Basic Biology (2016) |
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Principal Investigator |
TSUBOUCHI Hideo 東京工業大学, 科学技術創成研究院, 助教 (20283822)
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| Research Collaborator |
ARGUNHAN Bilge (30792759)
TSUBOUCHI Tomomi (70754505)
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 減数分裂 / 相同組換え / シナプトネマ複合体 / 染色体 / 細胞周期 / 染色体構造 / 出芽酵母 / 遺伝学 |
|---|
| Outline of Final Research Achievements |
The synaptonemal complex (SC) is a proteinaceous macromolecular assembly that forms during meiotic prophase I and mediates adhesion of paired homologous chromosomes. We showed that DDK (Dbf4-dependent Cdc7 kinase) is central to regulating SC destruction happening at the prophase I exit. Dbf4, the regulatory subunit of DDK, directly associates with and is phosphorylated by the Polo-like kinase Cdc5. In parallel, upregulated CDK1 activity also targets Dbf4. SC destruction relieved meiotic inhibition of the ubiquitous recombinase Rad51, suggesting that the mitotic recombination machinery is reactivated following prophase I exit to repair any persisting meiotic DNA double-strand breaks. We propose that the concerted action of DDK, Polo-like kinase, and CDK1 promotes efficient SC destruction at the end of prophase I to ensure faithful inheritance of the genome.
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