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RNA-Seq and ChIP Seq analysis of the Cu metalloregulatory transcription factor Cuf1 in Cryptococcus neoformans in response to Cu availability

ABSTRACT: RNA-Seq and ChIP Seq analysis of the Cu metalloregulatory transcription factor Cuf1 in Cryptococcus neoformans in response to Cu availability

PROVIDER: PRJNA432913 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6671130.fastq.gz	Fastqsanger.gz
	SRR6671140_1.fastq.gz	Fastqsanger.gz
	SRR6671140_2.fastq.gz	Fastqsanger.gz
	SRR6671121.fastq.gz	Fastqsanger.gz
	SRR6671131.fastq.gz	Fastqsanger.gz

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ChIP Seq analysis of the Cu metalloregulatory transcription factor Cuf1 in Cryptococcus neoformans in response to Cu availability

Project description:The essential yet toxic nature of Cu ions in living cells requires exquisite control of Cu homeostasis. The fungal pathogen C. neoformans regulates Cu homeostasis for survival during a complex host colonization process. During pulmonary infection host innate immune cells use Cu in an attempt to toxify C. neoformans, which responds by activating expression of Cu detoxifying proteins. However, during brain colonization expression of the fungal Cu import machinery is activated and required for virulence. To achieve the genetic plasticity required for adaptation to a continuum of distinct Cu environments within the host, C. neoformans utilizes the Cu-responsive transcription factor, Cuf1. Cuf1 is unique as it senses and responds to both high and low Cu environments, activating different sets of genes dependent on environmental Cu status. Cells lacking Cuf1 are compromised for colonization of the lungs and brain, highlighting Cuf1 as an important virulence factor. A genome-wide assessment of the Cuf1 binding sites in the genome of C. neoformans driven by Cu status identified novel genes required for adaptation to high and low Cu environments. These genes and their regulation provide new insights with respect to adaptive responses to changes in host Cu availability and could reveal new targets for therapeutic intervention in cryptococcosis.

2018-10-29 | GSE110120 | GEO

ChIP Seq analysis of the Cu metalloregulatory transcription factor Cuf1 in Cryptococcus neoformans in response to Cu availability

Project description:ChIP Seq analysis of the Cu metalloregulatory transcription factor Cuf1 in Cryptococcus neoformans in response to Cu availability

| PRJNA432922 | ENA

Global transcriptional analysis of wild-type and cuf1Δ Cryptococcus neoformans cells in responses to copper availability

Project description:The essential yet toxic nature of Cu ions in living cells requires exquisite control of Cu homeostasis. The fungal pathogen C. neoformans regulates Cu homeostasis for survival during a complex host colonization process. During pulmonary infection host innate immune cells use Cu in an attempt to toxify C. neoformans, which responds by activating expression of Cu detoxifying proteins. However, during brain colonization expression of the fungal Cu import machinery is activated and required for virulence. To achieve the genetic plasticity required for adaptation to a continuum of distinct Cu environments within the host, C. neoformans utilizes the Cu-responsive transcription factor, Cuf1. Cuf1 is unique as it senses and responds to both high and low Cu environments, activating different sets of genes dependent on environmental Cu status. Cells lacking Cuf1 are compromised for colonization of the lungs and brain, highlighting Cuf1 as an important virulence factor. In this study, we provide a genome-wide assessment of the Cuf1-dependent transcription changes driven by Cu status identified novel genes required for adaptation to high and low Cu environments. These genes and their regulation provide new insights with respect to adaptive responses to changes in host Cu availability and could reveal new targets for therapeutic intervention in cryptococcosis.

2018-10-29 | GSE110121 | GEO

Ribosome profiling of Cryptococcus neoformans H99

Project description:We measured protein translation (by ribosome profiling) and RNA levels (by polyA-enriched RNA-seq) in Cryptococcus neoformans strain H99 and Cryptococcus neoformans strain JEC21. This is the first transcriptome-wide map of translation in this species complex.

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Cryptococcus neoformans LC-MS/MS

Project description:Cryptococcus neoformans is an invasive human fungal pathogen, which causes pneumonia and meningoencephalitis in both healthy and immunodeficient individuals, resulting 181,100 deaths each year. Studies have demonstrated that copper detoxification machineries play critical functions in modulating C. neoformans fitness and pathogenicity in the host lung tissue. Pulmonary C. neoformans infection provokes the generation of toxic copper bombardment, which in return activate detoxification process in fungal cells. However, the molecular mechanism on how Cu inhibits C. neoformans in proliferation remains unclear. Here, using Cu detoxification gene knockout strains we demonstrated that exogenous Cu ions inhibit cell growth of the metallothionein mutant, which was significantly rescue when supplementing with the ROS scavenger, N-acetylcysteine. To future characterize the molecular mechanism of C. neoformans response to Cu toxicity, we employ iTRAQ with LC-MS/MS analysis, in the presence of exogenous Cu or NAC. Our data showed that an increased Cu level repressed expression of factors involved in protein translation but activates expression of important players in ubiquitin-degradation process. We proposed that the downregulation of protein synthesis and the upregulation of protein degradation were the main strategy of Cu toxicity. The metallothionein mutant showed a higher ubiquitination level under Cu treatment. In addition, MG132 could partially restore the Cu toxicity effect on metallothionein mutant. These results shed new light on the Cu antifungal mechanisms from proteomic profile.

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Transcriptomics analysis of amphotericin B and lactoferrin drug synergy in Cryptococcus neoformans H99

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 in Cryptococcus neoformans H99.

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Global proteomic analysis in Cryptococcus neoformans

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2024-05-23 | PXD033626 | Pride

Characterization of Alveolar macrophage subsets infected by Cryptococcus neoformans [ATAC-seq]

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