| Project/Area Number |
26860296
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
Minoru Nagi 国立感染症研究所, 真菌部, 研究員 (60711687)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | マイトファジー / ATG32 / オートファジー / 病原真菌 / 酵母 / ミトコンドリア / Candida glabrata / 病原性 / カンジダ / 鉄欠乏 / Candida |
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| Outline of Final Research Achievements |
The Screening of mitophagy activation conditions indicated that mitophagy was induced in Candida glabrata cells under iron-poor conditions, and that the disruption of ATG32, which is responsible for mitophagy in Saccharomyces cerevisiae, blocked mitophagy in C. glabrata. Unexpectedly, the mitophagy-deficient mutant of C. glabrata (atg32Δ) exhibited decreased longevity under iron-depleted conditions. The mitochondrial membrane potential in atg32Δ cells was significantly lower than that in wild-type (WT) cells under iron-depleted conditions. In a mouse model of disseminated infection, the atg32Δ strain resulted in significantly decreased kidney and spleen fungal burdens compared with WT strain. These results indicate that mitophagy in C. glabrata occurs in an iron-poor host tissue environment, and it may contribute to the longevity of cells through mitochondrial quality control, and to their pathogenesis.
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