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Antifungal drug responses in two Candida glabrata strains

ABSTRACT: Antifungal drug responses in two Candida glabrata strains

PROVIDER: PRJNA1141509 | ENA |

REPOSITORIES: ENA

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Antifungal drug responses in two Candida glabrata strains

Project description:Transcriptomic responses of Candida glabrata strains, BG2 and CBS138, to two azole antifungal drugs, Fluconazole and Voriconazole.

2025-07-29 | GSE273379 | GEO

Set1-mediated histone H3K4 methylation is conserved and required for azole induction of ergosterol biosynthesis genes and antifungal drug resistance in Candida glabrata

Project description:Fungal infections are a major health concern because of limited antifungal drugs and development of drug resistance. Candida can develop azole drug resistance by overexpression of drug efflux pumps or mutating ERG11, the target of azoles. However, the role of epigenetic histone modifications in azole-induced gene expression and drug resistance is poorly understood in Candida glabrata. In this study, we show that Set1 mediates histone H3K4 methylation in C. glabrata. In addition, loss of SET1 and histone H3K4 methylation increases azole susceptibility in both C. glabrata and S. cerevisiae. This increase in azole susceptibility in S. cerevisiae and C. glabrata strains lacking SET1 is due to distinct mechanisms. For S. cerevisiae, loss of SET1 decreased the expression and function of the efflux pump Pdr5, but not ERG11 expression under azole treatment. In contrast, loss of SET1 in C. glabrata does not alter expression or function of efflux pumps. However, RNA sequencing revealed that C. glabrata Set1 is necessary for azole-induced expression of all 12 genes in the late ergosterol biosynthesis pathway, including ERG11 and ERG3. Furthermore, chromatin immunoprecipitation analysis shows histone H3K4 trimethylation increases upon azole-induced ERG gene expression. In addition, high performance liquid chromatography analysis indicated Set1 is necessary for maintaining proper ergosterol levels under azole treatment. Clinical isolates lacking SET1 were also hypersusceptible to azoles which is attributed to reduced ERG11 expression but not defects in drug efflux. Overall, Set1 contributes to azole susceptibility in a species-specific manner by altering the expression and consequently disrupting pathways known for mediating drug resistance.

2022-07-28 | GSE209637 | GEO

Limosilactobacillus fermentum Limits Candida glabrata Growth by Ergosterol Depletion

Project description:Candida glabrata is a human-associated opportunistic fungal pathogen. It shares its niche with Lactobacillus spp. in the gastrointestinal and vaginal tract. In fact, Lactobacillus species are thought to competitively prevent Candida overgrowth. We investigated the molecular aspects of this antifungal effect by analyzing the interaction of C. glabrata strains with Limosilactobacillus fermentum. From a collection of clinical C. glabrata isolates, we identified strains with different sensitivities to L. fermentum in coculture. We analyzed the variation of their expression pattern to isolate the specific response to L. fermentum. C. glabrata-L. fermentum coculture induced genes associated with ergosterol biosynthesis, weak acid stress, and drug/chemical stress. L. fermentum coculture depleted C. glabrata ergosterol. The reduction of ergosterol was dependent on the Lactobacillus species, even in coculture with different Candida species. We found a similar ergosterol-depleting effect with other lactobacillus strains (Lactobacillus crispatus and Lactobacillus rhamosus) on Candida albicans, Candida tropicalis, and Candida krusei. The addition of ergosterol improved C. glabrata growth in the coculture. Blocking ergosterol synthesis with fluconazole increased the susceptibility against L. fermentum, which was again mitigated by the addition of ergosterol. In accordance, a C. glabrata Derg11 mutant, defective in ergosterol biosynthesis, was highly sensitive to L. fermentum. In conclusion, our analysis indicates an unexpected direct function of ergosterol for C. glabrata proliferation in coculture with L. fermentum.

2023-02-08 | GSE202656 | GEO

Histone Acetylation Regulator Gcn5 Mediates Drug Resistance and Virulence of Candida glabrata

Project description:This study explored the transcriptional change of Candida glabrata cells due to GCN5 deletion. We also compared the transcriptional responses to fluconazole and micafungin in WT and gcndelta cells relative to respective no drug controls.

2022-01-28 | GSE194310 | GEO

Comparative proteomics of pan-antifungal drug-resistant and drug-sensitive Candida auris

Project description:Whole cell proteomics of pan-antifungal drug resistant and sensitive Candida auris

2025-07-14 | PXD048342 | Pride

Translation Regulation Promotes Stress Adaptation in Candida glabrata

Project description:Candida glabrata is an important human fungal pathogen leading cause of non-albicans Candida infections. C. glabrata exhibits resistance to key antifungal drugs, rapidly replicates and divides in host macrophages and withstands highly stressful host conditions. This study explores the molecular mechanisms underlying stress adaptations in C. glabrata that contribute to its pathogenicity. Our findings revealed that C. glabrata survives oxidative stress and amino acid starvation more effectively than S. cerevisiae, C. albicans, and C. auris. We noted that Gcn2 kinase and Gcn4 play critical roles in this adaptation as Gcn2 phosphorylates eIF2α and downregulates the global protein translation, activating GCN4. RNA sequencing of WT and gcn4 mutant revealed that GCN4 activation during stress orchestrates the expression of stress-responsive genes vital for survival during amino acid starvation and oxidative stress. Ultimately assisting in the stress adaptative transcriptome. Thus, this study highlights the critical role of the Gcn2–Gcn4 pathway in stress adaptation in C. glabrata.

2025-07-14 | GSE283533 | GEO

Candida glabrata haploid and diploid

Project description:The different expression of Candida glabrata haploid and diploid.

2021-04-30 | GSE173617 | GEO

Homo sapiens whole blood infected with Candida spp. (here: Candida glabrata)

Project description:Homo sapiens fresh whole blood was infected with Candida glabrata. RNA-pool of both species extracted at 0min (control), 15, 30, 60, 120, 240 min. Samples are rRNA depleted. Measurement of Candida glabrata gene expression.

2018-12-26 | GSE114175 | GEO

RNA-Seq analysis of Candida glabrata wild-type and Cgset4Δ mutant in the presence and absence of the cell wall targeting echinocandin antifungal drug, caspofungin.

Project description:To determine the effect of caspofungin (CSP) treatment and/or loss of the SET domain-containing CgSet4 protein on the transcriptional response of log-phase C. glabrata cells. RNA-Seq analysis was conducted on CAA medium-grown log-phase Candida glabrata wild-type (wt) and CgSET4-deleted (Cgset4D) cells in the presence and absence of caspofungin.

2022-09-12 | GSE202654 | GEO

Secretome analysis of Candida glabrata wild-type and aspartyl protease-deficient strains

Project description:The project is aimed at characterizing the secretome of a human opportunistic fungal pathogen Candida glabrata. Additionally, the effect of loss of a family of eleven aspartyl proteases (Cg Yapsins) on the Candida glabrata secretome is studied.

2019-10-25 | PXD015131 | Pride

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