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The genomic tandem quadruplication is associated with ketoconazole resistance of Malassezia pachydermatis

ABSTRACT: The genomic tandem quadruplication is associated with ketoconazole resistance of Malassezia pachydermatis

PROVIDER: PRJNA485318 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7664160_1.fastq.gz	Fastqsanger.gz
	SRR7664160_2.fastq.gz	Fastqsanger.gz
	SRR7664159_1.fastq.gz	Fastqsanger.gz
	SRR7664159_2.fastq.gz	Fastqsanger.gz

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The genomic tandem quadruplication is associated with ketoconazole resistance of Malassezia pachydermatis

Project description:Purpose: Understanding the ketoconazole resistance mechanism in Malassezia pachydermatis Methods: The transcriptome profile of the ketoconazole resistant M. pachydermatis KCTC 27587 cells compared to that of ketoconazole sensitive M. pachydermatis CBS 1879 cells were generated by RNA-Seq using Illumina HiSeq. Results: The expressions of genes in the region of quadruplicated chromosome 4 were up-regulated.

2019-02-07 | GSE118354 | GEO

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Genomic analysis of ketoconazole resistance in the dandruff-associated cutaneous yeast Malassezia restricta.

Project description:To understand ketoconazole resistance mechanism in M. restricta, we investigated differentially expressed genes in the azole resistant isolates using transcriptome profile. Transcriptomes of ketoconazole susceptible and resistant M. restricta cells in the absence and precence of ketoconazole were compared and analyzed by RNA sequencing.

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Metabolic reconstruction of lipid metabolism of Malassezia

Project description:Malassezia species are lipophilic and lipid dependent yeasts belonging to the human and animal microbiota. Typically, they are isolated from regions rich in sebaceous glands. They have been associated with dermatological diseases such as seborrheic dermatitis, tinea versicolor, atopic dermatitis, and folliculitis. Genome sequences of Malassezia globosa, Malassezia sympodialis, and Malassezia pachydermatis lack genes related to fatty acid synthesis. Here, lipid synthesis pathways of M. furfur, M. pachydermatis, M. globosa, M. sympodialis and an atypical variant of M. furfur were reconstructed using genome data and Constraints Based Reconstruction and Analysis. The metabolic reconstruction allowed us to predict variation in the fluxes of each reaction over the network to satisfy the biomass objective function. Proteomic profiling improved and validated the models through data integration. Results suggest that several mechanisms including steroid and butanoate metabolism explain the yeast’s growth under different lipid conditions. Flux differences were observed in production of riboflavin in M. furfur and the biosynthesis of glycerolipids in the atypical variant of M. furfur and Malassezia sympodialis.

2017-10-02 | PXD004523 | Pride

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Project description:Malassezia furfur and Malassezia Pachydermatis genome sequencing and assembly

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Malassezia

Project description:Malassezia furfur and Malassezia Pachydermatis genome sequencing and assembly

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Genomic analysis of ketoconazole resistance in the dandruff-associated cutaneous yeast Malassezia restricta.

Project description:Genomic analysis of ketoconazole resistance in the dandruff-associated cutaneous yeast Malassezia restricta.

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Genomic Multiplication and Drug Efflux Influence Ketoconazole Resistance in <i>Malassezia restricta</i>.

Project description:Malassezia restricta is an opportunistic fungal pathogen on human skin; it is associated with various skin diseases, including seborrheic dermatitis and dandruff, which are usually treated using ketoconazole. In this study, we clinically isolated ketoconazole-resistant M. restricta strains (KCTC 27529 and KCTC 27550) from patients with dandruff. To understand the mechanisms of ketoconazole resistance in the isolates, their genomes were sequenced and compared with the susceptible reference strain M. restricta KCTC 27527. Using comparative genome analysis, we identified tandem multiplications of the genomic loci containing ATM1 and ERG11 homologs in M. restricta KCTC 27529 and KCTC 27550, respectively. Additionally, we found that the copy number increase of ATM1 and ERG11 is reflected in the increased expression of these genes; moreover, we observed that overexpression of these homologs caused ketoconazole resistance in a genetically tractable fungal pathogen, Cryptococcus neoformans. In addition to tandem multiplications of the genomic region containing the ATM1 homolog, the PDR5 homolog, which encodes the drug efflux pump protein was upregulated in M. restricta KCTC 27529 compared to the reference strain. Biochemical analysis confirmed that drug efflux was highly activated in M. restricta KCTC 27529, implying that upregulation of the PDR5 homolog may also contribute to ketoconazole resistance in the strain. Overall, our results suggest that multiplication of the genomic loci encoding genes involved in ergosterol synthesis, mitochondrial iron metabolism, and oxidative stress response and overexpression of the drug efflux pumps are the mechanisms underlying ketoconazole resistance in M. restricta.

| S-EPMC7203472 | biostudies-literature

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