ArticleAntimicrobial agents and chemotherapy2013
Azole susceptibility and transcriptome profiling in Candida albicans mitochondrial electron transport chain complex I mutants.
Article in Antimicrobial agents and chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 91 citations in OpenAlex.
- Berberine as a Promising Antifungal Agent: Insights into Molecular Mechanisms and Therapeutic Potential.ACS omega · 2026Review
- Morphotype-specific susceptibility toMicrobiology spectrum · 2026Article
- Identification and characterization of a novel broad-spectrum antifungal compound targeting theMicrobiology spectrum · 2026Article
- Candida auris vacuolar calcium pump mediates fluconazole efflux and resistance evolution.Nature microbiology · 2026Article
- Uncovering the role of mitochondrial genome in pathogenicity and drug resistance in pathogenic fungi.Frontiers in cellular and infection microbiology · 2025Review
- Exploration of novel mechanisms of azole resistance inAntimicrobial agents and chemotherapy · 2024Article
- Metabolic homeostasis in fungal infections from the perspective of pathogens, immune cells, and whole-body systems.Microbiology and molecular biology reviews : MMBR · 2024Review
- Divergent mitochondrial responses and metabolic signal pathways secure the azole resistance in Crabtree-positive and negativeMicrobiology spectrum · 2024Article
- Mitochondria complex I deficiency in Candida albicans arrests the cell cycle at S phase through suppressive TOR and PKA pathways.FEMS yeast research · 2024Article
- Lethal metabolism of Candida albicans respiratory mutants.PloS one · 2024Article
- Article
- Recent Progress in Research on Mitochondrion-Targeted Antifungal Drugs: a Review.Antimicrobial agents and chemotherapy · 2023Review
- Visible-Light-Activated Molecular Machines Kill Fungi by Necrosis Following Mitochondrial Dysfunction and Calcium Overload.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The Metabolism of Susceptibility: Clearing the FoG Between Tolerance and Resistance inCurrent clinical microbiology reports · 2023Article
- Article
- Assessing Complex I (CI) Mitochondrial Subunit Protein Functions in Candida albicans.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Article
- Mitochondrial perturbation reduces susceptibility to xenobiotics through altered efflux in Candida albicans.Genetics · 2021Article
- Shared evolutionary footprints suggest mitochondrial oxidative damage underlies multiple complex I losses in fungi.Open biology · 2021Article
- Inhibition of Respiration of Candida albicans by Small Molecules Increases Phagocytosis Efficacy by Macrophages.mSphere · 2020Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction in pathogenic fungi or model yeast causes altered susceptibilities to antifungal drugs. Here we have characterized the role of mitochondrial complex I (CI) of Candida albicans in antifungal susceptibility. Inhibitors of CI to CV, except for CII, increased the susceptibility of both patient and lab isolates, even those with a resistance phenotype. In addition, in a C. albicans library of 12 CI null mutants, 10 displayed hypersusceptibility to fluconazole and were severely growth inhibited on glycerol, implying a role for each gene in cell respiration. We chose two other hypersusceptible null mutants of C. albicans, the goa1Δ and ndh51Δ mutants, for transcriptional profiling by RNA-Seq. Goa1p is required for CI activity, while Ndh51p is a CI subunit. RNA-Seq revealed that both the ndh51Δ mutant and especially the goa1Δ mutant had significant downregulation of transporter genes, including CDR1 and CDR2, which encode efflux proteins. In the goa1Δ mutant, we noted the downregulation of genes required for the biogenesis and replication of peroxisomes, as well as metabolic pathways assigned to peroxisomes such as β-oxidation of fatty acids, glyoxylate bypass, and acetyl coenzyme A (acetyl-CoA) transferases that are known to shuttle acetyl-CoA between peroxisomes and mitochondria. The transcriptome profile of the ndh51Δ mutant did not include downregulation of peroxisome genes but had, instead, extensive downregulation of the ergosterol synthesis gene family. Our data establish that cell energy is required for azole susceptibility and that downregulation of efflux genes may be an outcome of that dysfunction. However, there are mutant-specific changes that may also increase the susceptibility of both of these C. albicans mutants to azoles.
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