| Project/Area Number |
07806046
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied molecular and cellular biology
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| Research Institution | Teikyo University of Science & Technology |
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Principal Investigator |
OHSUMI Mariko Teikyo University of Science and Technology Associated Prof., 理工学部, 助教授 (40168927)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Yeast / S.cerevisiae / Vacuole / Antibiotics / 酵母 / 抗生物質 |
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| Research Abstract |
Most of the aminoglycoside antibiotics are known to inhibit bacterial translation by interacting with the 16 S ribosomal RNA,resulting misreading in bacteria or their cell-free system. Among these antibiotics, streptomycin, selectively affects bacterial ribosomes. While, wild-type yeast, Saccharomyces cerevisiae, is highly rersistant to this antibiotic. However, vacuole-defective mutants (class I vam) were turned out to be sensitive to it. This work aimed to elucidate the mode of action of antibiotics in eukaryotes and the role of vacuole in the resistance by genetic approach.
Total thirteen streptomycin-sensitive mutants were obtained from mutagenized yeast cells and they were crossed each other for genetic analyzes. All these mutations were recessive and classified into six complementation groups. Every mutants showed sensitive phenotype to aminoglycoside antibiotics selectively, but not to other type of drugs. We are now trying to get these genes by complementation of their sensitive phenotype. Recently we obtained one of genes and sequnce analysis revealed that it is identical to TRK1, which encodes a high affinity K^+-transporter of yeast. We are now studying the function of TRK1p on the drug resistance. Further studies of these genes and their products will reveal the action mechanisms of antibiotics in eukaryote.
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