| Project/Area Number |
09680627
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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 |
Functional biochemistry
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| Research Institution | Kyushu Institute of Technology |
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Principal Investigator |
NIKAWA Junichi Kyushu Institute of Technology Faculty of Computer Science and Systems Engineering, Associate Professor, 情報工学部, 助教授 (00134271)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Yeast / Inositol / TGFbeta receptor / 転写因子 |
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| Research Abstract |
We previously reported that thc Saccharomyces cerevisiae irel5 mutation results in an inositol-auxotiophic phenotype, and that human cDNAs, such as TGF^<beta> receptor-encoding cDNA, can suppress the irel5 mutation. In this study, we found that the gene responsible for the irel5 mutation is HAG 1, which encodes a transcription factor for KAR2, obtained by isolating a yeast single-copy suppressor gene and by performing complementation analysis. Sequencing analysis revealed that the mutant HAG I gene obtained from We ire 15 mutant contained an AAA codon at position 50 instead of the AGA coin observed in the wild-type gene, resulting in the altearition of the amino acid horn Aug to Lys. All human cDNAs and yeast multicopy suppressors, which had been isolated -as suppressors for the irel5 mutation, were able to suppress the inositol-auxotrophic phenotype but not the defect in KA R2 induction of the hac I-disrupted strain
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