ArticlePloS one2020
An Erg11 lanosterol 14-α-demethylase-Arv1 complex is required for Candida albicans virulence.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- In Vitro Screening of Short Synthetic Antimicrobial Peptides Toward Food-Relevant Microorganisms: Antifungal Activity and Molecular Docking Analysis.Microorganisms · 2026Article
- Insights intomSphere · 2026Article
- Synergistic Antifungal Effects of Honokiol and Fluconazole Against Oral Candida: Implications for Managing Drug-Resistant Infections.Clinical and experimental dental research · 2026Article
- Intensification of Invasive Fungal Infections and Exploration of Effective Antifungal Drug Delivery Formulations: A Detailed Review.Infectious disorders drug targets · 2025Review
- Role of ERG11 and MDR1 genes in cycloheximide and multidrug resistance in Candida species.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2024Article
- Roles for Structural Biology in the Discovery of Drugs and Agrochemicals Targeting Sterol 14α-Demethylases.Journal of fungi (Basel, Switzerland) · 2021Review
- The Effect of Honokiol on Ergosterol Biosynthesis and Vacuole Function inJournal of microbiology and biotechnology · 2020Article
- Arv1; a "Mover and Shaker" of Subcellular Lipids.Contact (Thousand Oaks (Ventura County, Calif.))Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Azole resistant fungal infections remain a health problem for the immune compromised. Current therapies are limited due to rises in new resistance mechanisms. Therefore, it is important to identify new drug targets for drug discovery and novel therapeutics. Arv1 (are1 are2 required for viability 1) function is highly conserved between multiple pathogenic fungal species. Candida albicans (C. albicans) cells lacking CaArv1 are azole hypersusceptible and lack virulence. Saccharomyces cerevisiae (S. cerevisiae) Scarv1 cells are also azole hypersusceptible, a phenotype reversed by expression of CaArv1, indicating conservation in the molecular mechanism for azole susceptibility. To define the relationship between Arv1 function and azole susceptibility, we undertook a structure/function analysis of ScArv1. We identified several conserved amino acids within the ScArv1 homology domain (ScAhd) required for maintaining normal azole susceptibility. Erg11 lanosterol 14-α-demethylase is the rate-limiting enzyme in sterol biosynthesis and is the direct target of azole antifungals, so we used our ScArv1 mutants in order to explore the relationship between ScArv1 and ScErg11. Specific ScArv1 mutants ectopically expressed from a low copy plasmid were unable to restore normal azole susceptibility to Scarv1 cells and had reduced Erg11 protein levels. Erg11 protein stability depended on its ability to form a heterodimeric complex with Arv1. Complex formation was required for maintaining normal azole susceptibility. Scarv1 cells expressing orthologous CaArv1 mutants also had reduced CaErg11 levels, were unable to form a CaArv1-CaErg11 complex, and were azole hypersusceptible. Scarv1 cells expressing CaArv1 mutants unable to interact with CaErg11 could not sustain proper levels of the azole resistant CaErg11Y132F F145L protein. Caarv1/Caarv1 cells expressing CaArv1 mutants unable to interact with CaErg11 were found to lack virulence using a disseminated candidiasis mouse model. Expressing CaErg11Y132F F145L did not reverse the lack of virulence. We hypothesize that the role of Arv1 in Erg11-dependent azole resistance is to stabilize Erg11 protein level. Arv1 inhibition may represent an avenue for treating azole resistance.
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