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The Candida albicans ζ-crystallin homolog Zta1 promotes resistance to oxidative stress.
Gandra, Rafael M; Johnson, Chad J; Nett, Jeniel E; Konopka, James B.
Afiliação
  • Gandra RM; Department of Microbiology and Immunology, Stony Brook University, Stony Brook, New York, United States of America.
  • Johnson CJ; University of Wisconsin-Madison, Department of Medicine.
  • Nett JE; University of Wisconsin-Madison, Department of Medicine.
  • Konopka JB; University of Wisconsin-Madison, Department of Medical Microbiology & Immunology.
bioRxiv ; 2023 Sep 06.
Article em En | MEDLINE | ID: mdl-37732195
ABSTRACT
The fungal pathogen Candida albicans is capable of causing lethal infections in humans. Its pathogenic potential is due in part to the ability to resist various stress conditions in the host, including oxidative stress. Recent studies showed that a family of four flavodoxin-like proteins (Pst1, Pst2, Pst3, Ycp4) that function as quinone reductases promotes resistance to oxidation and is needed for virulence. Therefore, in this study Zta1 was examined because it belongs to a structurally distinct family of quinone reductases that are highly conserved in eukaryotes and have been called the ζ-crystallins. The levels of Zta1 in C. albicans rapidly increased after exposure to oxidants, consistent with a role in resisting oxidative stress. Accumulation of reactive oxygen species was significantly higher in cells lacking ZTA1 upon exposure to quinones and other oxidants. Furthermore, deletion of ZTA1 in a mutant lacking the four flavodoxin-like proteins, resulted in further increased susceptibility to quinones, indicating that these distinct quinone reductases work in combination. These results demonstrate that Zta1 contributes to C. albicans survival after exposure to oxidative conditions, which increases the understanding of how C. albicans resists stressful conditions in the host.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article