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RNA-Seq of Aspergillus fumigatus mutants resistant to itraconazole

ABSTRACT: RNA-Seq of Aspergillus fumigatus mutants resistant to itraconazole

PROVIDER: PRJEB1586 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	ERR236979_1.fastq.gz	Fastqsanger.gz
	ERR236979_2.fastq.gz	Fastqsanger.gz
	ERR236980_1.fastq.gz	Fastqsanger.gz
	ERR236980_2.fastq.gz	Fastqsanger.gz
	ERR236981_1.fastq.gz	Fastqsanger.gz

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RNA-Seq of Aspergillus fumigatus mutants resistant to itraconazole, SYBARIS project.

Project description:Two mutant strains of Aspergillus fumigatus derived from strain A1160, HapB and 29.9, display resistance to the antifungal drug itraconazole. To understand what underlying transcriptional processes contribute to this resistance, A1160, HapB and 29.9 were cultured either in the presence or absence of itraconazole. RNA-sequencing was used to compare transcription profiles of each mutant strain with or without the drug, to A1160 with or without drug.

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Project description:<p>Aspergillus fumigatus is a notorious opportunistic pathogen that causes Invasive Aspergillosis (IA) infections with high mortality in immunosuppressed individuals. Long-term antifungal drug azole abuse in clinical treatment and agriculture renders it ineffectual or drug resistant. Drug resistance can relate to the cellular metabolites and corresponding gene transcription. In this study, through untargeted metabolomics and transcriptomics following itraconazole (ITC) treatment we identified two plasma membrane-localized polyamine transporters Aftpo3 and Afdur3, which were important for polyamine homeostasis and ITC susceptibility in A. fumigatus. In the absence of Aftpo3 or Afdur3, the levels of cytoplasm polyamines had a moderate increase, accompanied by resistance to ITC. In comparison, overexpression of Aftpo3 or Afdur3 induced drastic increase of polyamines, which were linked with the sensitivity to ITC. Accordingly, our study demonstrated that concentration-dependence of polyamines affected susceptibility of A. fumigatus to ITC, by scavenging reactive oxygen species (ROS) at a moderate concentration or generating ROS at a high concentration rather than drug transport.</p>

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