ChIP-Seq analysis of the iron regulatory transcription factors in Cryptococcus neoformans in response to iron availability
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ABSTRACT:
PROVIDER: PRJNA521528 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8551130.fastq.gz | Fastqsanger.gz | |||
| SRR8551131.fastq.gz | Fastqsanger.gz | |||
| SRR8551132.fastq.gz | Fastqsanger.gz | |||
| SRR8551133.fastq.gz | Fastqsanger.gz | |||
| SRR8551126.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Understanding the iron-responsive regulatory networks in Cryptococcus neoformans. Methods: The transcriptome profiles of the wild-type, cir1 mutant and hapX mutant were generated by RNA-seq using Illumina Hiseq, in triplicate. The transcriptome profiles of each mutant was compared with that of the wild-type strain. Results: The iron-responsive transcription factors, Cir1 and HapX, are major regulators for iron acquisition and metabolism in C. neoformans.
2020-02-16 | GSE126313 | GEO
Project description:Purpose: Defining the regulatory role of the transcription factors, Cir1 and HapX, in C. neoformans. Methods: Chromatin immunoprecipitation followed by high-throughput sequencing was performed using chromatin immunoprecipitated DNA from the strains Cir1-Flag and HapX-Flag grown in low- and high-iron condition. Results: Cir1 and HapX bind to the promoter region of the genes involved in iron acquisition and metabolism in C. neoformans.
2020-02-16 | GSE126312 | GEO
Project description:Transcriptome analysis of the iron regulatory transcription factors in Cryptococcus neoformans in response to iron availability
| PRJNA521527 | ENA
Project description:ChIP-Seq and RNA-Seq analysis of the iron regulatory transcription factors in Cryptococcus neoformans in response to iron availability
| PRJNA521524 | ENA
Project description:Transcriptome profiling of wild type and cfo1 mutant with fluconazole treatment in Cryptococcus neoformans var. grubii H99 Purpose: The goals of this study are to compare cfo1 mutant transcriptome profiling (RNA-seq) to wild-type with or without fluconazole treatment in Cryptococcus neoformans var. grubii H99. Methods: mRNA profiles of wild-type and cfo1 mutant with or without fluconazole treatment were generated by RNA-Seq, using Illumina GAIIx. The sequence reads that passed quality filters were mapped to reference genome and the normalized RPKM values were calculated by CLC Genomics Workbench. Results: Compared to wild-type, a number of genes were differentially expressed in the cfo1 mutant, especially genes involved in iron homeostasis and transport, ergosterol biosynthesis, mitochondrial function and respiration. Conclusions: Our data suggested reduced expression of the genes in the respiratory chain is the main reason for altered antifungal sensitivity of the cfo1 mutant. The results of our study revealed that iron uptake plays a key role in fluconazole sensitivity of C. neoformans.
2013-05-31 | GSE37875 | GEO
Project description:Minerals are essential for proper cell function. In infectious processes where both cells of the causative agent and the host itself are involved, competition for their acquisition is necessary. In this context, pathogenic fungi have developed machinery to ensure the acquisition of minerals and at the same time have perfected strategies that protect them from intoxication by excess of them. In eukaryotic cells, minerals are involved both in the respiratory chain and in cellular metabolisms, which in microorganisms are related to the expression of virulence factors, while in the host, they are related to the activation and regulation of the immune system In the activation of phagocytic cells, in addition, the host can regulate the availability of minerals, which has been called nutritional immunity. Cryptococcosis is an opportunistic mycosis, acquired by inhaling fungal propagules present in the environment; it is a potentially fatal infection that affects the lungs and the central nervous system, both in immunosuppressed and immunocompetent people. The infection is caused by two species, namely: Cryptococcus neoformans (var. grubii (serotype A), var. neoformans (serotype D) and a hybrid corresponding to serotype AD) and Cryptococcus gattii (serotypes B and C). These species present phenotypic, genotypic and epidemiological differences, as well as in their geographical distribution. In recent years, mechanisms for the acquisition of iron and copper, among other micronutrients, have been described in C. neoformans, as well as their relationship, both with the expression of genes associated with virulence factors, the interaction with different intracellular signaling pathways. , especially in routes involved in adaptation to environmental changes and stress conditions. The regulation of the acquisition of these minerals is mediated by several signaling pathways, as the Rim 101 pathway in C. neoformans is essential in adapting to the change in pH and is particular to fungal cells. Iron and copper have been related to the induction of virulence through the production of melanin, capsules and the formation of titan cells, as well as enzymes related to oxidation-reduction phenomena and other virulence factors, which can be regulated by the factor of RIM101 transcription, this pathway induces the expression of genes that encode an iron transporter and a permease (SIT1 and CFT1, respectively) and a copper transporter (CTR4). This enables the yeast to survive in the host because it can rapidly transition from a slightly acidic environment in the phagolysosome to a slightly alkaline environment such as cerebrospinal fluid and serum. For mycoses in general, alternative therapies have been proposed, where the regulation of the acquisition of minerals in the tissue environment during the establishment of the mycosis could be a mechanism to control the growth of the fungus. Therefore, the compression of the signaling networks will allow exploring new alternatives for the development of novel antifungal drugs as well as biological biomarkers, both for the diagnosis and for possible combined therapies at the nutritional immunology level that help prevent and anticipate management. Taking these antecedents into account, we consider it important to evaluate the effect of iron and copper in Colombian clinical isolates of C. neoformans for the prediction of new antifungal targets.
2022-02-16 | PXD021687 | Pride
Project description:Transcriptome profiling of wild type and cfo1 mutant with fluconazole treatment in Cryptococcus neoformans var. grubii H99 Purpose: The goals of this study are to compare cfo1 mutant transcriptome profiling (RNA-seq) to wild-type with or without fluconazole treatment in Cryptococcus neoformans var. grubii H99. Methods: mRNA profiles of wild-type and cfo1 mutant with or without fluconazole treatment were generated by RNA-Seq, using Illumina GAIIx. The sequence reads that passed quality filters were mapped to reference genome and the normalized RPKM values were calculated by CLC Genomics Workbench. Results: Compared to wild-type, a number of genes were differentially expressed in the cfo1 mutant, especially genes involved in iron homeostasis and transport, ergosterol biosynthesis, mitochondrial function and respiration. Conclusions: Our data suggested reduced expression of the genes in the respiratory chain is the main reason for altered antifungal sensitivity of the cfo1 mutant. The results of our study revealed that iron uptake plays a key role in fluconazole sensitivity of C. neoformans. mRNA profiles of wild-type and cfo1 mutant with fluconazole treatment were generated by RNA-Seq, using Illumina GAIIx.
2013-05-31 | E-GEOD-37875 | biostudies-arrayexpress
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.
2019-06-22 | GSE133125 | GEO
Project description:Fungal diseases are critical burdens on the global healthcare system, infecting over 25% of the world’s population. For the opportunistic fungal pathogen, Cryptococcus neoformans, infection leads to cryptococcosis; a disease enabled by elaboration of sophisticated virulence factors, including polysaccharide capsule, melanin, thermotolerance, and extracellular enzymes in the presence of the host. Conversely, the host protects itself from fungal invasion by regulating and sequestering transition metals (e.g., iron, zinc, copper) important for microbial growth and survival. Building upon knowledge of zinc transport regulation at the transcriptional level, here, we explore the intricate relationship between zinc availability and fungal virulence via mass spectrometry-based quantitative proteomics. We observe distinct protein-level responses to zinc-limited and -excess conditions through a shift of the proteome profile towards stress response and metal acquisition, including the upregulation of the zinc transporter, ZIP1. In addition, we reveal a novel connection among zinc availability, protein folding, capsule production, and virulence through the detection of a Wos2-like ortholog in the secretome under replete conditions. Overall, we provide new biological insight into cellular remodeling at the protein level of C. neoformans under regulated zinc conditions and uncover a novel connection between zinc availability and fungal virulence. These findings support the development of new antifungal strategies focused on the enhancement of nutritional immunity within the host.
2022-02-16 | PXD023204 | Pride
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.
2019-09-08 | GSE130375 | GEO