ArticleAntimicrobial agents and chemotherapy2012
Phytosphingosine-1-phosphate is a signaling molecule involved in miconazole resistance in sessile Candida albicans cells.
Article in Antimicrobial agents and chemotherapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 26 citations in OpenAlex.
- Fungal Sphingolipids: Biosynthesis Pathways, Structural Features and Biological Functions.Journal of fungi (Basel, Switzerland) · 2026Review
- Targeting fungal lipid synthesis for antifungal drug development and potentiation of contemporary antifungals.npj antimicrobials and resistance · 2025Review
- The experimentally evolved fluconazole-resistant clade II isolates of Candidozyma auris exhibit a distinct lipid compositional landscape, highlighting intraclade sphingolipid heterogeneity.FEMS yeast research · 2025Article
- Step-wise evolution of azole resistance through copy number variation followed by KSR1 loss of heterozygosity in Candida albicans.PLoS pathogens · 2024Article
- Sphingolipid diversity in Candida auris: unraveling interclade and drug resistance fingerprints.FEMS yeast research · 2024Article
- The Metabolism of Susceptibility: Clearing the FoG Between Tolerance and Resistance inCurrent clinical microbiology reports · 2023Article
- Untargeted metabolomics to evaluate antifungal mechanism: a study of Cophinforma mamane and Candida albicans interaction.Natural products and bioprospecting · 2023Article
- Article
- Repurposing FDA approved drugs against the human fungal pathogen, Candida albicans.Annals of clinical microbiology and antimicrobials · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Previous research has shown that 1% to 10% of sessile Candida albicans cells survive treatment with high doses of miconazole (a fungicidal imidazole). In the present study, we investigated the involvement of sphingolipid biosynthetic intermediates in this survival. We observed that the LCB4 gene, coding for the enzyme that catalyzes the phosphorylation of dihydrosphingosine and phytosphingosine, is important in governing the miconazole resistance of sessile Saccharomyces cerevisiae and C. albicans cells. The addition of 10 nM phytosphingosine-1-phosphate (PHS-1-P) drastically reduced the intracellular miconazole concentration and significantly increased the miconazole resistance of a hypersusceptible C. albicans heterozygous LCB4/lcb4 mutant, indicating a protective effect of PHS-1-P against miconazole-induced cell death in sessile cells. At this concentration of PHS-1-P, we did not observe any effect on the fluidity of the cytoplasmic membrane. The protective effect of PHS-1-P was not observed when the efflux pumps were inhibited or when tested in a mutant without functional efflux systems. Also, the addition of PHS-1-P during miconazole treatment increased the expression levels of genes coding for efflux pumps, leading to the hypothesis that PHS-1-P acts as a signaling molecule and enhances the efflux of miconazole in sessile C. albicans cells.
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