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Saccharomyces cerevisiae S288C

ABSTRACT: Transcriptome and network analyses in Saccharomyces cerevisiae reveal that amphotericin B and lactoferrin synergy disrupt metal homeostasis and stress response

PROVIDER: PRJNA318684 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3396390_1.fastq.gz	Fastqsanger.gz
	SRR3396390_2.fastq.gz	Fastqsanger.gz
	SRR3396400.fastq.gz	Fastqsanger.gz
	SRR3396410.fastq.gz	Fastqsanger.gz
	SRR3396381_1.fastq.gz	Fastqsanger.gz

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Saccharomyces cerevisiae S288c

Project description:Transcriptome and network analysis of amphotericin B and lactoferrin drug synergy in Saccharomyces cerevisiae reveals down-regulation of the stress response and dysregulation of zinc and iron homeostasis

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Transcriptome and network analyses in Saccharomyces cerevisiae reveal that amphotericin B and lactoferrin synergy disrupt metal homeostasis and stress response

Project description:Invasive fungal infections (IFIs) are difficult to treat. Few effective antifungal drugs are available and many have problems with toxicity, efficacy and drug-resistance. To overcome these challenges, existing therapies may be enhanced using more than one agent acting in synergy. Previously, we have found amphotericin B (AMB) and the iron chelator, lactoferrin (LF), were synergistic against Cryptococcus neoformans and Saccharomyces cerevisiae. This study investigates the mechanism of AMB+LF synergy, using RNA-seq and network analyses. Genes involved in iron homeostasis showed increased expression upon treatment with AMB alone. Unexpectedly, AMB+LF treatment did not lead to increased expression of iron or zinc homeostasis genes however we observed decreased expression of oxidative stress response genes. Addition of iron or zinc to AMB+LF treated cells did not rescue the synergy, supporting the likelihood that the mechanism of synergy involves more than iron and zinc chelation. We clustered genes based on patterns of co-expression and found by network analysis that many genes involved in iron and zinc homeostasis, which have dysregulated expression upon AMB+LF treatment, are targets of transcription factors Aft1p and Zap1p. Hypothesizing that these might play a key role in the synergistic response, knock-out mutants of Aft1 and Zap1 were tested for increased sensitivity to AMB and oxidative stress. Both mutants showed hypersensitivity towards these treatments. Our results suggest the mechanism of AMB+LF synergy involves disruption to oxidative stress response, in addition to chelation of iron and zinc. Since Zap1 is conserved in C. neoformans and contains a putative drug binding domain, we suggest novel Zap1 binding molecules could be combined with existing antifungals to serve as synergistic antifungal treatments for this species.

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