Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1094434 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28507911_1.fastq.gz | Fastqsanger.gz | |||
| SRR28507911_2.fastq.gz | Fastqsanger.gz | |||
| SRR28507912_1.fastq.gz | Fastqsanger.gz | |||
| SRR28507912_2.fastq.gz | Fastqsanger.gz | |||
| SRR28507913_1.fastq.gz | Fastqsanger.gz |
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Project description:Proper mitochondrial function is critical for the ability of the fungal pathogen Cryptococcus neoformans to cause disease. Mitochondrial dysfunction of WT cells treated with antimycin A or L-DOPA, or on cells lacking Cir1 is evident from this dataset. These experiments revealed influences on transcript levels of genes encoding Fe-S cluster assembly components and the response to oxidative stress in Cryptococcus neoformans.
2024-04-07 | GSE222564 | 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:Cryptococcus neoformans is a ubiquitous free-living soil yeast and opportunistic pathogen that causes ~223,100 cases of cryptococcal meningitis per year, killing over 180,000 people. The pathogenicity of C. neoformans relies on its adaptation to the host conditions. An important difference between its natural environment and the mammalian host is the concentration of CO2. CO2 levels in the host fluctuate around 5%, which is ~125-fold higher than in ambient air. We recently found that while clinical isolates are tolerant to host levels ofCO2, many environmental isolates are CO2-sensitive and virulence-attenuated in animal models. The genetic basis responsible for cryptococcal adaptation to high levels of CO2 is unknown. Here, we utilized quantitative trait loci (QTL) mapping with 374 progeny from a cross between a CO2-tolerant clinical isolate and a CO2-sensitive environmental isolate to identify genetic regions regulating CO2 tolerance. To identify specific quantitative trait genes (QTGs), we applied fine mapping through backcrossing and bulk segregant analysis coupled with pooled genome sequencing of near-isogenic progeny but with distinct tolerance levels to CO2. The roles of the identified QTGs in CO2 tolerance were verified by targeted gene deletion. We further demonstrated that virulence levels among near-isogenic strains in a murine model of cryptococcosis correlate with their levels of CO2 tolerance. Moreover, we discovered that sensitive strains may adapt in vivo to become more tolerant to increased CO2 levels and more virulent. These findings highlight the underappreciated role of the host CO2 tolerance and its importance in the ability of an opportunistic environmental pathogen to cause disease.
2024-08-09 | GSE260932 | GEO
Project description:Cryptococcus neoformans is an environmental fungus that causes an estimated 180,000 deaths annually and transitions from the external environment to the host environment to cause disease. CO2 concentrations in the atmosphere (0.04%) are dramatically lower than in mammalian tissues (5%). Environmental C. neoformans strains that cannot tolerate 5% CO2 are much less virulent than CO2-tolerant strains. Microevolution at elevated CO2generated loss-of-function mutations in the nucleotide binding protein Avc1 that confer CO2 tolerance to CO2-intolerant strains. Mechanistically, Avc1 positively regulates the expression of plasma membrane transporters including PDR9, a phospholipid floppase that negatively modulates CO2 fitness. Deletion of AVC1 in five CO2-intolerant environmental strains increased competitive fitness in host CO2 and in a mouse infection model. Importantly, strains with similar AVC1 mutations have emerged in patients with relapsed cryptococcosis. Therefore, this microevolutionary convergence strongly suggests that adaptation to host CO2 is a significant driver of C. neoformans fitness during infection.
2025-02-24 | GSE284927 | GEO
Project description:Investigation of CO2 tolerance in the global pathogen Cryptococcus neoformans
| PRJNA1014009 | ENA
Project description:CircRNAs are a recently well-known regulator that mediates a variety of biological processes. Cryptococcus neoformans is an environmental fungal pathogen that can cause fatal cryptococcal meningitis in immunocompromised individuals. However, the involvement of circRNA in cryptococcal infection remains unclear. In this study, high‐throughput microarray was performed to identify the circRNA expression profile in cryptococcal meningitis patients.
2020-12-07 | GSE159601 | GEO
Project description:Carbon dioxide (CO2) sensing, transport, and metabolism play a pivotal role in survival and proliferation of pathogenic microbes infecting human host from natural environments due to the drastic difference of CO2 levels. Carbonic anhydrases (CAs) are not only key CO2-metabolic enzymes catalyzing reversible interconversion between CO2 and bicarbonate (HCO3-), but also important CO2-signaling modulators. Cryptococcus neoformans that causes fatal fungal meningitis contains two functional CAs, Can1 and Can2, among which Can2 plays essential roles for growth and sexual differentiation of the pathogen. However, downstream genes and signaling network regulated by CAs have not been studied thus far. In this study, we constructed a C. neoformans strain where CAN2 expression is controlled by the CTR4 (copper transporter) promoter and elucidated its transcriptome patterns by using DNA microarray analysis to elucidate downstream target genes of Can2. Expectedly, the CAN2 promoter replacement strain showed growth defects in a CO2-dependent manner when CAN2 is repressed. The CA-transcriptome analysis discovered a number of Can2-dependent genes, including those involved in fatty acid biosynthesis (FAS1), sexual differentiation (GPB1), capsule structure organization (CAS3), iron-metabolism (CFO2), and a number of stress-regulated genes, including an oxidative stress-responsive Atf1 transcription factor, although a majority of them do not have any orthologs in other fungi. The present study revealed other roles of Atf1 in capsule and melanin production and diverse stress responses, including thermotolerance and antifungal drug resistance, of C. neoformans. This study provides further insights into the signaling network of CA/CO2-sensing pathway in pathogenic fungi.
2010-06-01 | GSE21192 | GEO
Project description:The human fungal pathogen Cryptococcus neoformans undergoes many phenotypic changes to promote its survival in specific ecological niches and inside the host. To explore the role of chromatin remodeling on the expression of virulence-related traits, we identified and deleted seven genes encoding predicted class I/II histone deacetylases (HDACs) in the C. neoformans genome. Our results identified the HDA1 HDAC gene as a central mediator controlling several cellular processes, including mating and virulence. A global gene expression profile comparing the hda1Δ mutant versus wild-type revealed altered transcription of specific genes associated with the most prominent virulence attributes in this fungal pathogen. This study directly correlates the effects of Class I/II HDAC-mediated chromatin remodeling on the marked phenotypic plasticity and virulence potential of this microorganism. Furthermore, our results provide insights into regulatory mechanisms involved in virulence gene expression that are likely shared with other microbial pathogens.
2018-06-06 | GSE109582 | GEO
Project description:In eukaryotes, inositol polyphosphates perform essential metabolic and signaling functions. Using human fungal pathogen Cryptococcus neoformans as a model, we created mutants in three inositol polyphosphates kinases: Arg1, Ipk1 and Kcs1. Each of the mutants produces a unique repertoire of inositol polyphosphates, different from the wild type strain. Comparative phenotypic and transcriptome analyses of wild type and mutant strains indicates that inositol polyphosphate PP-IP5 (IP7) is the key regulator of gene expression, fitness and virulence in C. neoformans.
2016-03-03 | GSE78824 | GEO
Project description:We report that TNFalpha mediated dendritic cell priming via alterations in histone 3 lysine 4 trimethylation (H3K4me3) sustains lasting protective Th1/Th17 responses during invasive Cryptococcus neoformans pulmonary infection. Cryptococcus neoformans pulmonary infection results in increased global lung dendritic cell H3K4me3 over naive lung dendritic cells. Blockage of TNFalpha during Cryptococcus neoformans pulmonary infection results in decreased H3K4me3 at sites crucial to protective Th1/Th17 responses.
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