| Project/Area Number |
11102002
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| Research Category |
Grant-in-Aid for Specially Promoted Research
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YAMAMOTO Masayuki The University of Tokyo, Graduate School of Science, Professor, 大学院・理学系研究科, 教授 (40114706)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Kayoko The University of Tokyo, Graduate School of Science, Research Associate, 大学院・理学系研究科, 助手 (80345264)
KARASHIMA Takeshi The University of Tokyo, Graduate School of Science, Research Associate, 大学院・理学系研究科, 助手 (30323497)
WATANABE Yoshinori The University of Tokyo, Graduate School of Science, Associate Professor, 大学院・理学系研究科, 助教授 (20212326)
YAMASHITA Akira The University of Tokyo, Molecular Genetics Research Laboratory, Research Associate, 遺伝子実験施設, 助手 (30312276)
杉本 亜砂子 東京大学, 大学院・理学系研究科, 助手 (80281715)
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| Project Period (FY) |
1999 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥322,900,000 (Direct Cost: ¥280,000,000、Indirect Cost: ¥42,900,000)
Fiscal Year 2003: ¥52,000,000 (Direct Cost: ¥40,000,000、Indirect Cost: ¥12,000,000)
Fiscal Year 2002: ¥62,400,000 (Direct Cost: ¥48,000,000、Indirect Cost: ¥14,400,000)
Fiscal Year 2001: ¥71,500,000 (Direct Cost: ¥55,000,000、Indirect Cost: ¥16,500,000)
Fiscal Year 2000: ¥55,000,000 (Direct Cost: ¥55,000,000)
Fiscal Year 1999: ¥82,000,000 (Direct Cost: ¥82,000,000)
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| Keywords | MEIOSIS / FISSION YEAST / WORM / MEIOTIC DIVISION / mRNA / STABILITY / TOR KINASE / NUCLEAR MORPHOLOGY / RNA結合タンパク質 / プロテインフォスファターゼ / セントロメア / 精子形成 / 転写因子 / cAMP / プロテインキナーゼ / 14-3-3タンパク質 / コヒーシン / 還元分裂 / RNAi / 核移行 / 14-3-3 / 卵形成 / 太糸期 |
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| Research Abstract |
1.We screened for suppressors of the fission yeast meiosis-defective mutant lacking meiRNA, which is indispensable for meiosis I, and isolated meiosis-specific genes mei4, spo5, ssm4 and others. It turned out that the suppression was caused not by their protein products but by part of their mRNAs. Interestingly, these mRNAs were unstable and did not accumulate in mitotically growing cells, even if artificially expressed, and the region responsible for this instability overlapped with the region that suppressed loss of meiRNA. Thus we speculate that these mRNAs carry a region that renders them unstable in the mitotic cell cycle, and that a certain mechanism operates to stabilize them during meiosis. 2.Fission yeast Mei2p, the regulator of the initiation of meiosis, forms a dot structure in prophase I nuclei. We have demonstrated that this dot is a complex of Mei2p and nascent meiRNA, just transcribed from the gene. 3.We isolate a new mutant of fission yeast tor1, which encodes a TOR kinase required for sexual development. We then isolated gad8, which encoded a kinase of the AGC family, as a suppressor of this mutant. Analysis has shown that Tor1p regulates sexual development and stress responses through Gad8p. 4.We isolated C. elegans DAZ-1, a homolog of DAZ responsible for azoospermia in mammals. In DAZ-1-defective worms, the meiotic process was arrested at pachytene during oogenesis. They showed abnormal nuclear morphology even in germ cells at the proliferative stage in the gonad. The DAZ-1-defective worms did not show expansion of nucleoli nor formation of the central cytoplasmic core in germ cells at the meiotic stage, and these cells appeared to be less active in protein synthesis. Other data have suggested that DAZ-1 may also be involved in switching sexuality of the gonad.
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