Cap1p attenuates the apoptosis of Candida albicans

Authors


Correspondence

Y. Wang or Y.-Y. Jiang, New Drug Research and Development Center, School of Pharmacy, Second Military Medical University, 325 Guohe Road, Shanghai 200433, China

Fax: +86 21 6549 0641

Tel: +86 21 8187 1359; +86 21 8187 1357

E-mails: wangyansmmu@126.com; jiangyuanying@126.com

Abstract

Candida albicans is the most common opportunistic fungal pathogen and its apoptosis is inducible by environmental stress. Based on our previous finding that transcription factor Cap1p was involved in baicalein-induced apoptosis, the present study aimed to further clarify the role of Cap1p in apoptosis by observing the impact of CAP1 deletion on cell fate. It was found that apoptotic stimulation with amphotericin B, acetic acid and hydrogen peroxide increased the number of apoptotic and necrotic cells, caspase activity and the accumulation of reactive oxygen species, whereas it decreased the mitochondrial membrane potential and intracellular ATP level in the cap1Δ/Δ mutant. The cell fate was, at least partly, caused by glutathione depletion and attenuation of the expression of the glutathione reductase gene in the cap1Δ/Δ mutant. Collectively, our data suggest that Cap1p participated in the apoptosis of C. albicans by regulating the expression of the glutathione reductase gene and glutathione content.

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