ArticleAntioxidants & redox signaling2013
Ybp1 and Gpx3 signaling in Candida albicans govern hydrogen peroxide-induced oxidation of the Cap1 transcription factor and macrophage escape.
Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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52 citing papers in PubMed, 80 citations in OpenAlex.
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- Vacuole and mitochondria patch (vCLAMP) protein Mcp1 reduces the pathogenesis of Candida albicans by impeding the function of Cap1-mediated oxidative stress response.BMC microbiology · 2026Article
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- A roadmap to chemically reactive species: how diverse oxidants affectMicrobiology and molecular biology reviews : MMBR · 2025Review
- Integrative Phosphoproteomic and Proteomic Analysis ofJournal of proteome research · 2025Article
- Hyphal swelling induced in the phagosome of macrophages.Fungal biology · 2024Article
- Candida albicans pathways that protect against organic peroxides and lipid peroxidation.PLoS genetics · 2024Article
- Carbon substrates promotes stress resistance and drug tolerance in clinical isolates of Candida tropicalis.Archives of microbiology · 2024Article
- Halofantrine Hydrochloride Acts as an Antioxidant Ability Inhibitor That Enhances Oxidative Stress Damage toAntioxidants (Basel, Switzerland) · 2024Article
- Systematic identification and characterization of five transcription factors mediating the oxidative stress response in Candida albicans.Microbial pathogenesis · 2024Article
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- Identification of glutathione metabolic genes from a dimorphic fungus Talaromyces marneffei and their gene expression patterns under different environmental conditions.Scientific reports · 2023Article
- Facile Synthesis of MagneticPharmaceutics · 2023Article
- The Role of the Glutathione System in Stress Adaptation, Morphogenesis and Virulence of Pathogenic Fungi.International journal of molecular sciences · 2022Review
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10 authors at 2 institutions in 1 country.
Funding
Abstract
aimsAs Candida albicans is the major fungal pathogen of humans, there is an urgent need to understand how this pathogen evades toxic reactive oxygen species (ROS) generated by the host immune system. A key regulator of antioxidant gene expression, and thus ROS resistance, in C. albicans is the AP-1-like transcription factor Cap1. Despite this, little is known regarding the intracellular signaling mechanisms that underlie the oxidation and activation of Cap1. Therefore, the aims of this study were; (i) to identify the regulatory proteins that govern Cap1 oxidation, and (ii) to investigate the importance of Cap1 oxidation in C. albicans pathogenesis.
resultsIn response to hydrogen peroxide (H2O2), but not glutathione-depleting/modifying oxidants, Cap1 oxidation, nuclear accumulation, phosphorylation, and Cap1-dependent gene expression, is mediated by a glutathione peroxidase-like enzyme, which we name Gpx3, and an orthologue of the Saccharomyces cerevisiae Yap1 binding protein, Ybp1. In addition, Ybp1 also functions to stabilise Cap1 and this novel function is conserved in S. cerevisiae. C. albicans cells lacking Cap1, Ybp1, or Gpx3, are unable to filament and thus, escape from murine macrophages after phagocytosis, and also display defective virulence in the Galleria mellonella infection model. INNOVATION: Ybp1 is required to promote the stability of fungal AP-1-like transcription factors, and Ybp1 and Gpx3 mediated Cap1-dependent oxidative stress responses are essential for the effective killing of macrophages by C. albicans.
conclusionActivation of Cap1, specifically by H2O2, is a prerequisite for the subsequent filamentation and escape of this fungal pathogen from the macrophage.
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