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Integrated transcriptomic analysis of Trichosporon asahii uncovers the core genes and pathways of fluconazole resistance

ABSTRACT: Integrated transcriptomic analysis of Trichosporon asahii uncovers the core genes and pathways of fluconazole resistance

OTHER RELATED OMICS DATASETS IN: GSE106454

PROVIDER: PRJNA416913 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6246430_1.fastq.gz	Fastqsanger.gz
	SRR6246430_2.fastq.gz	Fastqsanger.gz
	SRR6246431_1.fastq.gz	Fastqsanger.gz
	SRR6246431_2.fastq.gz	Fastqsanger.gz
	SRR6246432_1.fastq.gz	Fastqsanger.gz

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Integrated transcriptomic analysis of Trichosporon asahii uncovers the core genes and pathways of fluconazole resistance

Project description:We performed a series of fluconazole (FLC) perturbation experiments for two T. asahii strains, a clinical isolate stain CBS2479 (T2) and an environmental isolate strain CBS8904 (T8), to uncover potential genes and pathways involved in FLC resistance.

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Monocyte-like THP-1 Cells: Trichosporon asahii Infected vs Control

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Monocyte-like THP-1 Cells: Trichosporon asahii Infected vs Control

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Metabolome and transcriptome combined profiling reveals fluconazole resistance mechanisms of Trichosporon asahii and role of farnesol in fluconazole tolerance

Project description:Trichosporon asahii is a basidiomycete yeast that is pathogenic to humans and animals, and fluconazole-resistant strains have recently increased. Farnesol secreted by fungi is a factor that causes variations in fluconazole resistance; however, few studies have explored the underlying mechanisms. Therefore, this study aims to delineate the fluconazole resistance mechanisms of T. asahii and explore farnesol’s effects on these processes. A comparative metabolome-transcriptome analysis of untreated fluconazole-sensitive (YAN), fluconazole-resistant (PB) T. asahii strains and 25 μM farnesol-treated strains (YAN-25 and PB-25, respectively) was performed. The membrane lipid-related genes and metabolites were upregulated in the PB vs YAN and PB-25 vs PB comparisons. Farnesol demonstrated strain-dependent mechanisms underlying fluconazole tolerance between the YAN and PB strains, and upregulated and downregulated efflux pumps in PB-25 and YAN-25 strains, respectively. Membrane lipid-related metabolites were highly correlated with transporter-coding genes. Fluconazole resistance in T. asahii was induced by membrane lipid bio-synthesis activation. Farnesol inhibited fluconazole resistance in the sensitive strain, but enhanced resistance in the resistant strain by upregulating efflux pump genes and membrane lipids. This study offers valuable insights into the mechanisms underlying fungal drug resistance and provides guidance for future research aimed at developing more potent antifungal drugs for clinical use.

2023-11-20 | MTBLS7236 | MetaboLights

Integrated transcriptomic analysis of Trichosporon Asahii uncovers the core genes and pathways of fluconazole resistance.

Project description:Trichosporon asahii (T. asahii) has emerged as a dangerous pathogen that causes rare but life-threatening infections. Its resistance to certain antifungal agents makes it difficult to treat, especially for patients undergoing long-term antibiotic therapy. In this study, we performed a series of fluconazole (FLC) perturbation experiments for two T. asahii strains, a clinical isolate stain CBS 2479 (T2) and an environmental isolate strain CBS 8904 (T8), to uncover potential genes and pathways involved in FLC resistance. We achieved 10 transcriptomes of T2 and T8 that were based on dose and time series of FLC perturbations. Systematic comparisons of the transcriptomes revealed 32 T2 genes and 25 T8 genes that are highly sensitive to different FLC perturbations. In both T2 and T8 strains with the phenotype of FLC resistance, the processes of oxidation-reduction and transmembrane transport were detected to be significantly changed. The antifungal susceptibility testing of FLC and penicillin revealed their resistance pathways are merged. Accumulated mutations were found in 564 T2 and 225 T8 genes, including four highly mutated genes that are functionally related to the target of rapamycin complex (TOR). Our study provides abundant data towards genome-wide understanding of the molecular basis of FLC resistance in T. asahii.

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