Role of mitophagy of Candida glabrata in pathogenicity.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26860296
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Bacteriology (including mycology)
• Research Institution: National Institute of Infectious Diseases
• Principal Investigator: Minoru Nagi 国立感染症研究所, 真菌部, 研究員 (60711687)
• Project Period (FY): 2014-04-01 – 2017-03-31
• 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

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.

Free Research Field

医真菌学、分子生物学、生化学