Ontology highlight
ABSTRACT:
PROVIDER: PRJNA639838 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12026117_1.fastq.gz | Fastqsanger.gz | |||
| SRR12026117_2.fastq.gz | Fastqsanger.gz | |||
| SRR12026118_1.fastq.gz | Fastqsanger.gz | |||
| SRR12026118_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29627: Chromosome copy number variation in Cryptococcus neoformans influences virulence and occurs in isolates from AIDS patients: CBS7779 black and white strains GSE29671: Chromosome copy number variation in Cryptococcus neoformans influences virulence and occurs in isolates from AIDS patients: clinal and environmental strains Refer to individual Series
2011-05-31 | E-GEOD-29675 | biostudies-arrayexpress
Project description:The adaptation of fungal pathogens to the host environment via large-scale genomic changes is a poorly characterized phenomenon. We recently discovered clinical strains of Cryptococcus neoformans, the leading cause of fungal meningoencephalitis in HIV/AIDS patients, which are disomic for chromosome 13. In the current study, we examined the relationship between disomy, expression of the virulence factor melanin and virulence in a mouse model of cryptococcosis. We found that melanin production was correlated with monosomy at chromosome 13, and that disomic variants were less melanized and attenuated for virulence in mice. Changes in the copy number of other chromosomes were also detected in strains showing variation in melanin formation after growth in culture and after passage through mice. A survey of environmental and clinical isolates maintained in culture revealed few occurrences of disomic chromosomes. However, an examination of isolates that were freshly collected from the cerebral spinal fluid of AIDS patients and minimally cultured provided evidence for mixed infections and copy number variation. Overall, these results suggest that the genome of C. neoformans exhibits a greater degree of plasticity than previously appreciated. Importantly, genome variation is associated with virulence factor expression and disease severity, and its occurrence in isolates from AIDS patients suggests that it may have clinical relevance. Genome comparison of clinal and environmental strains vs standard strain H99
2011-05-31 | E-GEOD-29671 | biostudies-arrayexpress
Project description:The adaptation of fungal pathogens to the host environment via large-scale genomic changes is a poorly characterized phenomenon. We recently discovered clinical strains of Cryptococcus neoformans, the leading cause of fungal meningoencephalitis in HIV/AIDS patients, which are disomic for chromosome 13. In the current study, we examined the relationship between disomy, expression of the virulence factor melanin and virulence in a mouse model of cryptococcosis. We found that melanin production was correlated with monosomy at chromosome 13, and that disomic variants were less melanized and attenuated for virulence in mice. Changes in the copy number of other chromosomes were also detected in strains showing variation in melanin formation after growth in culture and after passage through mice. A survey of environmental and clinical isolates maintained in culture revealed few occurrences of disomic chromosomes. However, an examination of isolates that were freshly collected from the cerebral spinal fluid of AIDS patients and minimally cultured provided evidence for mixed infections and copy number variation. Overall, these results suggest that the genome of C. neoformans exhibits a greater degree of plasticity than previously appreciated. Importantly, genome variation is associated with virulence factor expression and disease severity, and its occurrence in isolates from AIDS patients suggests that it may have clinical relevance.
2011-06-01 | GSE29671 | GEO
Project description:The adaptation of fungal pathogens to the host environment via large-scale genomic changes is a poorly characterized phenomenon. We recently discovered clinical strains of Cryptococcus neoformans, the leading cause of fungal meningoencephalitis in HIV/AIDS patients, which are disomic for chromosome 13. In the current study, we examined the relationship between disomy, expression of the virulence factor melanin and virulence in a mouse model of cryptococcosis. We found that melanin production was correlated with monosomy at chromosome 13, and that disomic variants were less melanized and attenuated for virulence in mice. Changes in the copy number of other chromosomes were also detected in strains showing variation in melanin formation after growth in culture and after passage through mice. A survey of environmental and clinical isolates maintained in culture revealed few occurrences of disomic chromosomes. However, an examination of isolates that were freshly collected from the cerebral spinal fluid of AIDS patients and minimally cultured provided evidence for mixed infections and copy number variation. Overall, these results suggest that the genome of C. neoformans exhibits a greater degree of plasticity than previously appreciated. Importantly, genome variation is associated with virulence factor expression and disease severity, and its occurrence in isolates from AIDS patients suggests that it may have clinical relevance.
2011-05-31 | GSE29627 | GEO
Project description:The adaptation of fungal pathogens to the host environment via large-scale genomic changes is a poorly characterized phenomenon. We recently discovered clinical strains of Cryptococcus neoformans, the leading cause of fungal meningoencephalitis in HIV/AIDS patients, which are disomic for chromosome 13. In the current study, we examined the relationship between disomy, expression of the virulence factor melanin and virulence in a mouse model of cryptococcosis. We found that melanin production was correlated with monosomy at chromosome 13, and that disomic variants were less melanized and attenuated for virulence in mice. Changes in the copy number of other chromosomes were also detected in strains showing variation in melanin formation after growth in culture and after passage through mice. A survey of environmental and clinical isolates maintained in culture revealed few occurrences of disomic chromosomes. However, an examination of isolates that were freshly collected from the cerebral spinal fluid of AIDS patients and minimally cultured provided evidence for mixed infections and copy number variation. Overall, these results suggest that the genome of C. neoformans exhibits a greater degree of plasticity than previously appreciated. Importantly, genome variation is associated with virulence factor expression and disease severity, and its occurrence in isolates from AIDS patients suggests that it may have clinical relevance. Genome comparison of CBS7779 black and white strains vs standard strain H99
2011-05-30 | E-GEOD-29627 | biostudies-arrayexpress
Project description:Cryptococcus neoformans causes meningoencephalitis and is an increasing human health threat. C. neoformans is neurotropic, and persists in the cerebrospinal fluid (CSF) of the mammalian host during infection. In order to survive in the host, pathogenic fungi must procure nutrients such as carbon and nitrogen. To enhance our understanding of nutrient acquisition during infection by Cryptococcus species, we examined utilization of nitrogen sources available in CSF. We screened for growth and capsule production of 817 global environmental and clinical isolates on various sources of nitrogen. Capsule production was assessed using ammonium and urea in the presence or absence of benomyl to determine the relationship of urea exposure to capsule production. Since urea is metabolized to ammonia and CO2 (a known signal for capsule induction), we examined urea metabolism mutants for their response to urea regarding capsule production. Non-preferred nitrogen sources were found to greatly affect capsule production in pathogenic species of Cryptococcus. Urea induced the greatest magnitude of capsule production. Capsule induction by urea was greater in Cryptococcus gattii strains than in C. neoformans strains. In addition, both environmental and clinical strains grew robustly on uric acid, casamino acids, creatinine, and asparagine as sole nitrogen sources. While substantial growth on nitrate was not apparent at day 3, growth was apparent by day 6 for all serotypes. In this study, transcription profiles of urea pathway mutants (ure1 and amt1/2) and WT Cryptococcus neoformans strains were compared in a dye-swap experiment following 1hr exposure to proline or proline + urea (.25g/L).
2013-09-25 | E-GEOD-46829 | biostudies-arrayexpress
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 causes meningoencephalitis and is an increasing human health threat. C. neoformans is neurotropic, and persists in the cerebrospinal fluid (CSF) of the mammalian host during infection. In order to survive in the host, pathogenic fungi must procure nutrients such as carbon and nitrogen. To enhance our understanding of nutrient acquisition during infection by Cryptococcus species, we examined utilization of nitrogen sources available in CSF. We screened for growth and capsule production of 817 global environmental and clinical isolates on various sources of nitrogen. Capsule production was assessed using ammonium and urea in the presence or absence of benomyl to determine the relationship of urea exposure to capsule production. Since urea is metabolized to ammonia and CO2 (a known signal for capsule induction), we examined urea metabolism mutants for their response to urea regarding capsule production. Non-preferred nitrogen sources were found to greatly affect capsule production in pathogenic species of Cryptococcus. Urea induced the greatest magnitude of capsule production. Capsule induction by urea was greater in Cryptococcus gattii strains than in C. neoformans strains. In addition, both environmental and clinical strains grew robustly on uric acid, casamino acids, creatinine, and asparagine as sole nitrogen sources. While substantial growth on nitrate was not apparent at day 3, growth was apparent by day 6 for all serotypes.
2013-09-25 | GSE46829 | GEO