Cap1p attenuates the apoptosis of Candida albicans

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 apoptos...

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Published inThe FEBS journal Vol. 280; no. 11; pp. 2633 - 2643
Main Authors Dai, Bao‐Di, Wang, Yan, Zhao, Lan‐Xue, Li, De‐Dong, Li, Ming‐Bang, Cao, Yong‐Bing, Jiang, Yuan‐Ying
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.06.2013
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Summary: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. We investigated the role of Cap1p in apoptosis of Candida albicans and demonstrated that more apoptotic cells, more necrotic cells, decreased mitochondrial membrane potential and intracellular ATP level accompanied with increased caspase activity and ROS accumulation occurred in the cap1Δ/Δ mutant upon apoptotic stimuli. The cell fate of cap1Δ/Δ was, as least partly, caused by decreased glutathione and GLR1 expression.
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ISSN:1742-464X
1742-4658
DOI:10.1111/febs.12251