| Project/Area Number |
11480177
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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 |
Functional biochemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OHYA Yoshikazu The Univ. of Tokyo, Grand. Schl. Frontier Sci., Professor, 大学院・新領域創成科学研究科, 教授 (20183767)
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| Co-Investigator(Kenkyū-buntansha) |
SONOIKE Kintake The Univ. of Tokyo, Grand. Schl Frontier Sci., Asociate Professor, 大学院・新領域創成科学研究科, 助教授 (30226716)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥16,000,000 (Direct Cost: ¥16,000,000)
Fiscal Year 2001: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2000: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥10,300,000 (Direct Cost: ¥10,300,000)
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| Keywords | cell wall / yeast / GTPase / genetics / intragenic complementation / GTPase / 形態形成 / 細胞膜 / グルカン合成酵素 / ゲラニルゲラニル化 / Rho GTPase / call-1 |
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| Research Abstract |
In many eukaryotic organisms, Rho-type small GTPases are involved in the determinations of cell polarity and cell morphology. Rholp, one of the essential Rho-type small GTPases in the yeast Saccharomyces cerevisiae, is a multifunctional molecular switch involved in establishment of cell morphogenesis. We characterized systematically isolated temperature-sensitive mutations in the RH01 gene and identified two groups of rhol mutations (rholA and rholB) possessing distinct functional defects. Biochemical and cytological analyzes demonstrated that mutant cells of the rholA and rholB groups have defects in activation of Rholp effectors, Pkc1p kinas and 1, 3-β-glean syntheses (GS), respectively. Heteroallelic diploid strains with rholA and rholB mutations are able to grow even at the restrictive temperature of the corresponding homoallelic diploid strains, showing intragenic complementation. The ability to activate both of the essential Rholp rho1p proteins is restored in the heteroallelic diploid. Thus, each of the complementing rhol mutation groups abolishes a distinct function of Rho1p, activation of Pck1p kinase or GS activity.
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