Transcriptomic changes in response to host temperature stress in the pathogen Crypococcus neoformans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA496032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8042980.fastq.gz | Fastqsanger.gz | |||
| SRR8042990.fastq.gz | Fastqsanger.gz | |||
| SRR8042971.fastq.gz | Fastqsanger.gz | |||
| SRR8042981.fastq.gz | Fastqsanger.gz | |||
| SRR8042991.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Using RNA-seq we report the global changes that occur in response to host temperature stress in the pathogen, Crypococcus neoformans, and reveal that mRNA decay plays a critical role in the transcriptomic and translatomic reprogramming necessary for stress adaptation.
2019-09-26 | GSE121183 | GEO
Project description:Cryptococcus spp. are environmental fungi that first must adapt to the host environment before they can cause life-threatening meningitis in immunocompromised patients. Host CO2 concentrations are 100-fold higher than the external environment and strains unable to grow at host CO2 concentrations are not pathogenic. Using a genetic screening and transcriptional profiling approach, we found that the TOR pathway is critical for C. neoformans adaptation to host CO2 partly through Ypk1-dependent remodeling of phosphatidylserine asymmetry at the plasma membrane. We also identified a C. neoformans ABC/PDR transporter (PDR9) that is highly expressed in CO2-sensitive environmental strains, suppresses CO2-induced phosphatidylserine remodeling, and increases susceptibility to host concentrations of CO2. Interestingly, regulation of plasma membrane lipid asymmetry by the TOR-Ypk1 axis is distinct in C. neoformans compared to S. cerevisiae. Finally, host CO2 concentrations suppress the C. neoformans pathways that respond to host temperature (Mpk1) and pH (Rim101), indicating that host adaptation requires a stringent balance among distinct stress responses.
2023-10-24 | GSE241788 | GEO
Project description:Ubiquitination is a reversible protein modification involved in various cellular processes in eukaryotic cells. Deubiquitinating enzymes, the proteins responsible for the removal of ubiquitin, act as essential regulators to maintain ubiquitin homeostasis and to exquisitely regulate protein degradation via the ubiquitination pathway. Cryptococcus neoformans is an important basidiomycete pathogen that causes life-threatening meningoencephalitis primarily within the immunocompromised population. In order to understand the possible influence deubiquitinating enzymes have on growth and virulence of the model pathogenic yeast Cryptococcus neoformans, we generated deletion mutants of 7 putative deubiquitinase genes. Compared to other deubiquitinating enzyme mutants, a ubp5∆ mutant exhibited severely attenuated virulence and many distinct phenotypes, including decreased capsule formation, hypomelanization, defective sporulation, and elevated sensitivity to several external stressors (such as high temperature, oxidative and nitrosative stresses, high salts, and antifungal agents). Ubp5 appears to be the major deubiquitinating enzyme in C. neoformans for maintaining a pool of free ubiquitin for stress responses, supports the evolutionary divergence of Cryptococcus sp. from the model yeast S. cerevisiae, and provides an important paradigm for understanding the potential role of deubiquitination in virulence by other pathogenic fungi. In addition, other putative deubiquitinase mutants (doa4∆ and ubp13∆) exhibit similar phenotypes to the ubp5∆ mutant, illustrating possible functional overlap among deubiquitinating enzymes in C. neoformans. Certain functioning deubiquitinating enzymes are essential for the virulence composite of C. neoformans and provide an additional yeast survival and propagation advantage in the host.
2012-04-11 | GSE35067 | GEO
Project description:Analysis of ccr4 Delta vs. wild type shifted from 30oC to 37oC for 10 minutes To determine the effect of ccr4 deletion on temperature stress-responsive changes in gene expression in C. neoformans
2011-07-11 | GSE28592 | GEO
Project description:Ubiquitination is a reversible protein modification involved in various cellular processes in eukaryotic cells. Deubiquitinating enzymes, the proteins responsible for the removal of ubiquitin, act as essential regulators to maintain ubiquitin homeostasis and to exquisitely regulate protein degradation via the ubiquitination pathway. Cryptococcus neoformans is an important basidiomycete pathogen that causes life-threatening meningoencephalitis primarily within the immunocompromised population. In order to understand the possible influence deubiquitinating enzymes have on growth and virulence of the model pathogenic yeast Cryptococcus neoformans, we generated deletion mutants of 7 putative deubiquitinase genes. Compared to other deubiquitinating enzyme mutants, a ubp5M-bM-^HM-^F mutant exhibited severely attenuated virulence and many distinct phenotypes, including decreased capsule formation, hypomelanization, defective sporulation, and elevated sensitivity to several external stressors (such as high temperature, oxidative and nitrosative stresses, high salts, and antifungal agents). Ubp5 appears to be the major deubiquitinating enzyme in C. neoformans for maintaining a pool of free ubiquitin for stress responses, supports the evolutionary divergence of Cryptococcus sp. from the model yeast S. cerevisiae, and provides an important paradigm for understanding the potential role of deubiquitination in virulence by other pathogenic fungi. In addition, other putative deubiquitinase mutants (doa4M-bM-^HM-^F and ubp13M-bM-^HM-^F) exhibit similar phenotypes to the ubp5M-bM-^HM-^F mutant, illustrating possible functional overlap among deubiquitinating enzymes in C. neoformans. Certain functioning deubiquitinating enzymes are essential for the virulence composite of C. neoformans and provide an additional yeast survival and propagation advantage in the host. In this study, transcription profiles of ubp5 mutant and WT Cryptococcus neoformans strains were compared in a dye-swap experiment following 1hr exposure to either 30C or 37C.
2012-04-10 | E-GEOD-35067 | biostudies-arrayexpress
Project description:Cryptococcus neoformans is a type of pathogenic fungi that can cause infections in people with weakened immune systems. This fungal pathogen can survive in the body by growing at the host's body temperature (37\'b0C), forming a carbohydrate capsule, and producing melanin. When Cryptococcus neoformans strains lack certain septin proteins, they cannot grow at 37\'b0C and are not able to cause infections in mice. However, it is not yet clear how septins help the yeast to grow at the host's body temperature. Septins are a group of proteins that are important for cell division and morphogenesis. In the model organism, Saccharomyces cerevisiae septins are essential. S. cerevisiae septins form a higher-order complex at the mother bud-neck to scaffold over 80 proteins, including those involved in cell wall organization, cell polarity, and cell cycle control. In C. neoformans, septins also form a complex at the mother bud neck but the septin interacting proteome in this species remains largely unknown. In this study, the entire septin complex in C. neoformans was uncovered as downregulated during the stationary growth phase and heat stress. In addition, we investigated the septin interactome in C. neoformans, shedding light on the proteins that interact with septins Cdc3 and Cdc10 under ambient temperature and heat stress, respectively. Our findings unveiled a diverse array of interacting proteins, including components of Golgi to plasma membrane transport, cell division, and single-stranded DNA binding. \'a0Overall, this study delineates septins in C. neoformans as part of the cytoskeleton and cytoskeleton-dependent cytokinesis and provides a landscape of septin interactors to investigate and further understand septin biology in fungal systems.
2024-10-28 | PXD052407 | Pride
Project description:Cryptococcus neoformans is a fungal pathogen with a polysaccharide capsule that becomes greatly enlarged in the mammalian host and during in vitro growth in response to host-like conditions. To understand how individual host-like signals affect capsule size and gene expression, we grew cells with and without all combinations of 5 signals suspected of affecting capsule size: Tissue-culture medium (DMEM or RPMI), temperature (37°C), CO2 (5%), and the addition of HEPES buffer. For each combination of conditions, we grew cultures with or without exogenous cAMP, and sampled cells for RNA-Seq at 0, 30, 90, 180, 1440 minutes and for measurement of capsule thickness at 1440 min. We also took samples for RNA-Seq at 30, 90, 180, 1440 minutes and carried out RNA-Seq in quadruplicate.
2023-08-02 | GSE226255 | GEO
Project description:Analysis of ccr4 Delta vs. wild type shifted from 30oC to 37oC for 10 minutes To determine the effect of ccr4 deletion on temperature stress-responsive changes in gene expression in C. neoformans Replicate cultures of the wild type (Control) and ccr4Delta mutant were grown to mid log phase at 30oC, harvested and resuspended in 37oC pre-warmed medium for 10 minutes. Pooled biological replicate cultures were hybridized in duplicate (2 slides, 2 arrays/slide)
2011-07-11 | E-GEOD-28592 | biostudies-arrayexpress
Project description:Human infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
2014-12-31 | GSE57720 | GEO
Project description:Cryptococcus neoformans is a fungal pathogen with a polysaccharide capsule that becomes greatly enlarged in the mammalian host and during in vitro growth in response to host-like conditions. To understand how individual host-like signals affect capsule size and gene expression, we grew wild-type cells and cells lacking components of the cAMP pathway: Pde1, Pde2, Pkr1. We also took samples for RNA-Seq at 30, 90, 180, 1440 minutes and carried out RNA-Seq in quadruplicate. We also measured capsule thickness at 1440 min.
2023-08-02 | GSE226651 | GEO