| Project/Area Number |
06660088
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
応用微生物学・応用生物化学
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
NAKAJIMA Tasuku Tohoku University, Faculty of Agriculture, Department of Applied Biological Chemistry, Assistant professor, 農学部, 助教授 (20091720)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | killer toxin / yeast cell wall / killer toxin resistant gene / beta-1,3-glucan / ベータ1, 3グルカン / ベータ1,3グルカン / 酵母の遺伝子 |
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| Research Abstract |
HM-1killer toxin secreted from Hansenula mrakii inhibits the growth of Saccharomyces cerevisiae cells by interfering with beta-1,3-glucan synthesis. A gene whose overexpression can endow Saccharomyces cerevisiae cells with resistant to HM-1 killer toxin was cloned. The gene, designated HKR1 contains 5.4-kb open reading frame. The HKR1 encodes a serine-and threonine-rich type 1 membrane protein with calcium-binding consensus sequence in the cytoplasmic domein. The null mutation of HKR1 is lethal and overexpression of HKR1 increases beta-1,3-glucan contents in cell wall. The partial disruption of HKR1 significantly reduced the level of beta-1,3-glucan synthase activities as well as cell wall beta-1,3-glucan contents, and altered the axial budding pattern of haploid cells. Immunofluorescednce microscopy with an antibody raised against Hkr1 expreseed in Escherichia coli revealed that HKR1 was predominantly localized on the cell surface. These results demonstrate that HKR1 encodes a cell surfase protein that regulates both cell wall beta-1,3-glucan synthesis and budding pattern.
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