| Project/Area Number |
25252065
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | Nara Institute of Science and Technology |
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Principal Investigator |
Takagi Hiroshi 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (50275088)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAMOTO Susumu 千葉大学, 真菌医学研究センター, 教授 (80125921)
CHIBANA Hiroji 千葉大学, 真菌医学研究センター, 准教授 (30333488)
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| Research Collaborator |
WATANABE Daisuke
NASUNO Ryo
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| Project Period (FY) |
2013-10-21 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥44,070,000 (Direct Cost: ¥33,900,000、Indirect Cost: ¥10,170,000)
Fiscal Year 2015: ¥10,790,000 (Direct Cost: ¥8,300,000、Indirect Cost: ¥2,490,000)
Fiscal Year 2014: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2013: ¥21,580,000 (Direct Cost: ¥16,600,000、Indirect Cost: ¥4,980,000)
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| Keywords | 酵母 / 一酸化窒素 / 酸化ストレス / シグナル伝達 / 病原真菌 / ストレス耐性 / 酸化ストレス耐性 |
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| Outline of Final Research Achievements |
The flavoprotein Tah18 is involved in NO synthase (NOS)-like activity and Tah18-dependent NO synthesis confers high-temperature stress tolerance on the budding yeast Saccharomyces cerevisiae. We showed that NOS-like activity requiring Tah18 induced cell death upon treatment with H2O2. Our findings indicate that the Tah18-Dre2 complex regulates cell death as a molecular switch via Tah18-dependent NOS-like activity in response to oxidative stresses. We also studied the antioxidative mechanism by NO. NO increased the transcription of the CTR1 gene encoding copper transporter, the intracellular copper content, the activity of superoxide dismutase Sod1, and the cell viability in a manner dependent on Mac1. Thus, Tah18-dependent NO synthesis exhibits dual effects, cell protection and death, in yeast. Our results also suggest that NO is involved in the growth, infection and pathogenicity of the pathogenic yeasts and fungi, Candida glabrata, Cryptococcus neoformans and Aspergillus fumigatus.
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