| Project/Area Number |
13043036
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Hiroshima University |
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Principal Investigator |
HIRATA Dai Hiroshima University, Graduate School of Advanced Science of Matter, Professor, 大学院先端物質科学研究科, 教授 (30243603)
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| Project Period (FY) |
2001 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥37,700,000 (Direct Cost: ¥37,700,000)
Fiscal Year 2005: ¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 2004: ¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 2003: ¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 2002: ¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 2001: ¥7,700,000 (Direct Cost: ¥7,700,000)
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| Keywords | checkpoint / cell polarity / cell cycle / cell morphogenesis / yeast / 細胞周期 / M期開始 / 情報伝達 / チェックポイント / 細胞極性 / 成長極性 |
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| Research Abstract |
Regulation of the onset of mitosis is important for checkpoint control and stress response. In this research, we studied a checkpoint monitoring cell polarity in fission and G2-M regulation by signaling pathways in budding yeast.
Our findings are as follows.
1. A checkpoint monitoring cell polarity in fission yeast
(1) We showed that the fission yeast Funy-like protein Mor2 is required for cell polarity control and is localized to the cell ends and septum, and that the mor2 mutation disrupts the localization of F-actin, inducing a Weel-dependent G2-delay (EMBO J. 2002). Our results indicated that fission yeast cells have a novel checkpoint monitoring cell polarity. (2) We found that the conserved proteins, MO25-like Pmo25, GC kinase Nak1, Mor2, and NDR kinase Orb6, constitute a morphogenesis network (MOR) that is important for cell polarity and cell separation, and that the septation intiation network (SIN) regulates locaization of Pmo25 to SPB and the Nak1-Orb6 kinase activities during early interphase (EMBO J. 2005).
2. G2-M regulation by signaling pathways in budding yeast :
(1) We showed that the addition of ethanol causes Swe1-depdent G2 delay with a transient dispersion of F-actin cytoskeleton, resulting in an increase in cell size (Biosci. Biotechnol. Biochem. 2002). (2) We identified the SAH1 gene encoding S-adenosyl-L-homocysteine hydrolase as a mutation that suppressed the calcium-sensitive phenotypes of the zdsl-deleted cells, and showed that S-adenosylmethionine is involved in GI cell-cycle regulation (Proc. Nati. Acad. Sci. USA 2002). (3) We found antagonistic regulation of G2-M regulation and cell polarity control by the calcineurin and HOG-MAPK pathways (J. Biol. Chem. 2004). (4) We showed that Pkc1 is important for sustaining Cln2 level and polarized bud growth in response to calcium signal (J. Cell Sci. 2005).
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