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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

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

Project description:Transcriptional profiling of Monocyte-like THP-1 Cells with Trichosporon asahii Infected THP-1 Cells comparing untreated THP-1 cells Two-condition experiment,Trichosporon asahii Infected THP-1 Cells vs THP-1 Cells. Biological replicates: 3 infected THP-1 Cells, independently grown and harvested.One replicate per array.

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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.

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