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ABSTRACT: Study on antifungal mechanism of quaternary ammonium salt

PROVIDER: PRJNA791525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17303234_1.fastq.gz	Fastqsanger.gz
	SRR17303234_2.fastq.gz	Fastqsanger.gz
	SRR17303235_1.fastq.gz	Fastqsanger.gz
	SRR17303235_2.fastq.gz	Fastqsanger.gz
	SRR17303236_1.fastq.gz	Fastqsanger.gz

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Project description:Copper-azole based formulations were widely used against fungal decay for preservation of wood timbers. While efficient for wood protection, leaching of both copper and azole within the environment has deleterious impact on soils and surface waters. Moreover, no recycling process is currently available for these wood waste. By taking advantage of the fact that certain fungi have the capacity to cope with these active compounds, we propose that some ligninolytic fungi could be good biocatalysts for detoxifying copper-azole formulations. Using the white-rot fungus Phanerochaete chrysosporium as a model, we demonstrated that the main strategies implemented by this fungus to counteract the antifungal effect of the product, in particular azoles, are the modulation of the lipids and sterols content, the maintenance of DNA integrity, detoxification of azoles by extracellular degradation likely through the Fenton chemistry, biosorption at the cell wall, efflux, and intracellular detoxification by the three-step detoxification pathway. By using comparative transcriptomics between a copper-azole formulation and a copper-quaternary ammonium formulation, we manage to identify genes specifically involved in azole resistance and detoxification within this complex system, opening perspectives for both the identification of key molecular players that could be the targets for developing long-term acquired antifungal resistance mechanisms, and the management of azoles residues by mycoremediation processes.

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Project description:Eupolauridine and liriodenine are plant-derived aporphinoid alkaloids that exhibit potent inhibitory activity against the opportunistic fungal pathogens Candida albicans and Cryptococcus neoformans. However, the molecular mechanism of this antifungal activity is unknown. In this study, we show that eupolauridine 9591 (E9591), a synthetic analog of eupolauridine, and liriodenine methiodide (LMT), a methiodide salt of liriodenine, mediate their antifungal activities by disrupting mitochondrial iron-sulfur (Fe-S) cluster synthesis. Several lines of evidence supported this conclusion. First, both E9591 and LMT elicited a transcriptional response indicative of iron imbalance, causing the induction of genes that are required for iron uptake and for the maintenance of cellular iron homeostasis. Second, a genome-wide fitness profile analysis showed that yeast mutants with deletions in iron homeostasis–related genes were hypersensitive to E9591 and LMT. Third, treatment of wild-type yeast cells with E9591 or LMT generated cellular defects that mimicked deficiencies in mitochondrial Fe-S cluster synthesis, including an increase in mitochondrial iron levels, a decrease in the activities of Fe-S cluster enzymes, a decrease in respiratory function, and an increase in oxidative stress. Collectively, our results demonstrate that E9591 and LMT perturb mitochondrial Fe-S cluster biosynthesis; thus, these two compounds target a cellular pathway that is distinct from the pathways commonly targeted by clinically used antifungal drugs. Therefore, the identification of this pathway as a target for antifungal compounds has potential applications in the development of new antifungal therapies.

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