| Project/Area Number |
14370518
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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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| Research Field |
Urology
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| Research Institution | NAGOYA CITY UNIVERSITY |
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Principal Investigator |
HAYASHI Yutaro Nagoya City University, Graduate School of Medical Sciences, Associate professor, 大学院・医学研究科, 助教授 (40238134)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Yoshihiro Nagoya City University, Graduate School of Medical Sciences, Reserch Associate, 大学院・医学研究科, 助手 (40244561)
MURAKAMI Hiroshi Nagoya City University, Graduate School of Medical Sciences, Associate professor, 大学院・医学研究科, 助教授 (80262020)
NAKANISHI Makoto Nagoya City University, Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (40217774)
KOHRI Kenjiro Nagoya City University, Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (30122047)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | meiosis / DNA damaae checkpoint / fission yeast / 細胞周期 |
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| Research Abstract |
Molecular mechanism in human meiosis is still unknown as no effective methods are established to analyze. We examined checkpoint system to DNA damage during fission yeast meiosis.
In vegetative cdsl cells, checkpoint Rad (Rad1, Rad3 etc.) dependent activation of Chk1 in response to hydroxyurea(HU) arrest the cell cycle in G2. But Chk1 dependent response to HU during meiosis is attenuated. To investigate the existence of meiotic DNA damage checkpoint system, rad1, chk1, cds1 mutants are treated with alkylating agent methylmethane sulfonate(MMS; 0.01%) during early meiosis. These mutants undergo aberrant chromosomal segregation, delayed and abnormal meiotic divisions at s similar rate to wild type. In meiotic cds1 cells with MMS, subtle phosphorylation in Chk1 protein is observed in immunoblot, compared to the vegetative cells. Cdc2-Tyr15 in meiotic S phase is also dephosphorylated. The DNA damage response of checkpoint mutants to MMS in this study suggests DNA damage checkpoint in fission yeast meiosis is attenuated or not in existence.
Recently, other groups have demonstrated that spontaneous S phase damage is repaired by activating recombination without checkpoint arrest. It is not shown whether the checkpoint aberration causes meiotic abnormality in human. As some genes related to the DNA recombination have already identified in human, it would be significant to examine the genes to know the molecular mechanism in meiosis.
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