ArticleAntimicrobial agents and chemotherapy2015
Sphingolipids mediate differential echinocandin susceptibility in Candida albicans and Aspergillus nidulans.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Sphingolipid Metabolism in Oral Diseases: Pathogenic Mechanisms, Biomarkers, and Therapeutic Opportunities.Biomedicines · 2026Review
- Molecular landscape of the fungal plasma membrane and implications for antifungal action.Nature communications · 2025Article
- Tn-seq screens inmSphere · 2025Article
- The Gcn5 lysine acetyltransferase mediates cell wall remodeling, antifungal drug resistance, and virulence ofmSphere · 2025Article
- Evolutionary dynamics in gut-colonizing Candida glabrata during caspofungin therapy: Emergence of clinically important mutations in sphingolipid biosynthesis.PLoS pathogens · 2024Article
- What 'Omics can tell us about antifungal adaptation.FEMS yeast research · 2022Review
- Oceanapiside, a Marine Natural Product, Targets the Sphingolipid Pathway of Fluconazole-ResistantMarine drugs · 2021Article
- Fungal Resistance to Echinocandins and the MDR Phenomenon inJournal of fungi (Basel, Switzerland) · 2018Review
- Review
- The Rim Pathway Mediates Antifungal Tolerance in Candida albicans through Newly Identified Rim101 Transcriptional Targets, Including Hsp90 and Ipt1.Antimicrobial agents and chemotherapy · 2018Article
- Aspergillus fumigatusAntimicrobial agents and chemotherapy · 2018Article
- Critical role for CaFEN1 and CaFEN12 of Candida albicans in cell wall integrity and biofilm formation.Scientific reports · 2017Article
- Article
- Characterization of AnNce102 and its role in eisosome stability and sphingolipid biosynthesis.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The cell wall synthesis-inhibiting echinocandins, including caspofungin and micafungin, play important roles in the treatment of candidiasis and aspergillosis. Previous studies revealed that, in the haploid yeast Candida glabrata, sphingolipid biosynthesis pathway mutations confer caspofungin reduced susceptibility (CRS) but micafungin increased susceptibility (MIS). Here, we describe one Candida albicans strain (of 10 tested) that similarly yields CRS-MIS mutants at relatively high frequency. Mutants demonstrated increased levels of long-chain bases (sphingolipid pathway intermediates) and, unique to this strain, loss of His104/Pro104 heterozygosity in the TSC13-encoded enoyl reductase. CRS-MIS was similarly observed in a C. albicans homozygous fen1Δ fen12Δ laboratory strain and in diverse wild-type strains following exogenous long-chain-base treatment. Analogous to these results, CRS-MIS was demonstrated in an Aspergillus nidulans basA mutant encoding defective sphingolipid C4-hydroxylase and in its wild-type parent exposed to long-chain bases. Sphingolipids likely modulate echinocandin interaction with their Fks membrane target in all susceptible fungi, with potential implications for optimizing therapy with existing antifungals and the development of novel agents.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.