Cryptococcus neoformans
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ABSTRACT:
PROVIDER: PRJNA117961 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Understanding the regulatory role of Sre1 in Cryptococcus neoformans. Methods: The transcriptome profiles of the wild-type and sre1 mutant were generated by RNA-seq using Illumina Hiseq. The transcriptome profile of the sre1 mutant was compared with that of the wild-type strain. Results: The Sterol Regulatory Element Binding Protein, Sre1 is a major regulator for the genes involved in ergosterol biosynthetic pathway and iron acquisition in C. neoformans.
2020-09-01 | GSE135039 | GEO
Project description:Comparison of wild-type serotype A C. neoformans cells grown at 21% and 3% oxygen for 2 hours in rich medium. Also comparison of wild-type and Sre1-pathway mutant strains grown at 3 % oxygen for 2 hours in rich medium.
2009-09-29 | GSE18282 | GEO
Project description:Purpose: Defining the regulatory role of the transcription factor Sre1 in C. neoformans. Methods: Chromatin immunoprecipitation followed by high-throughput sequencing was performed using chromatin immunoprecipitated DNA from the strain Flag-Sre1 grown in low- and high-iron media under normoxia and hypoxia condition. Results: Sre1 directly bind to the promoter region of the genes involved in ergosterol biosynthetic pathway and iron acquisition in C. neoformans.
2020-09-01 | GSE135038 | GEO
Project description:Comparison of wild-type serotype A C. neoformans cells grown at 21% and 3% oxygen for 2 hours in rich medium. Also comparison of wild-type and Sre1-pathway mutant strains grown at 3 % oxygen for 2 hours in rich medium. Two-condition experiment. Each comparison was performed in two biological replicates, each containing duplicate probes/array (=4 data points total per comparison).
2010-05-22 | E-GEOD-18282 | 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:We investigated the effects of the hypoxia-mimetic CoCl2 on the gene expression of pathogenic fungus Cryptococcus neoformans. Keywords: compound treatment design
2009-05-01 | GSE11390 | GEO
Project description:The target of rapamycin (TOR) pathway is an evolutionarily conserved signal transduction system that is activated by varying nutrient and environmental signals and governs a plethora of eukaryotic biological processes. Nevertheless, its role in the human fungal pathogen Cryptococcus neoformans remains elusive. In this study, we investigated the TOR pathway by functionally characterizing two Tor-like kinases, Tor1 and Tlk1, in C. neoformans. We successfully deleted TLK1, but not TOR1. TLK1 deletion did not result in any evident in vitro phenotypes, except for a minor role in diamide and polyene resistance, suggesting that Tlk1 is mainly dispensable for the growth of C. neoformans. We further demonstrated that Tor1, but not Tlk1, is essential and the target of rapamycin by constructing and analyzing conditionally regulated strains and sporulation analysis of heterozygous mutants in the diploid strain background. To analyze the functions of Tor1 in more detail, we constructed constitutive TOR1 overexpression strains. Tor1 negatively regulated thermotolerance and the DNA damage response, which are two important virulence factors of C. neoformans. We also found that TOR1 overexpression reduced Mpk1 phosphorylation, which is required for cell wall integrity and thermoresistance, and Rad53 phosphorylation, which governs the DNA damage response pathway. Tor1 is localized to the cytoplasm but enriched in the vacuole membrane. Phosphoproteomics and transcriptomics revealed that Tor1 regulates a variety of biological processes, including metabolic processes, cytoskeleton organization, ribosome biogenesis, autophagy, and stress response. Finally, screening rapamycin-sensitive and -resistant kinase and transcription factor mutants revealed that the TOR pathway may crosstalk with a number of signaling pathways, including the Hog1 pathway. In conclusion, our study demonstrates that a single Tor1 kinase plays a variety of roles in the fungal meningitis pathogen C. neoformans.
2019-10-10 | PXD012983 | Pride
Project description:The RNA interference (RNAi) mediated by homology-dependent degradation of the target mRNA with small RNA molecules plays a key role in controlling transcription and translation processes in a number of eukaryotic organisms. The RNAi machinery is also evolutionarily conserved in a wide variety of fungal species, including pathogenic fungi. To elucidate the physiological functions of the RNAi pathway in Cryptococcus neoformans that causes fungal meningitis, here we performed genetic analyses for genes encoding Argonaute (AGO1 and AGO2), RdRP (RDP1), and Dicers (DCR1 and DCR2) in both serotype A and D C. neoformans. The present study shows that Ago1, Rdp1, and Dcr2 are the major components of the RNAi process occurring in C. neoformans. However, the RNAi machinery is not involved in regulation of production of two virulence factors (capsule and melanin), sexual differentiation, and diverse stress response. To further gain insights into the global regulatory circuit governed by the RNAi pathway, comparative transcriptome analysis using the serotype A and D RNAi mutants was performed. Notably, an increase in transcript abundance of active transposons, such as T2 and T3, was observed in the rdp1? mutant. Therefore, this study can improve our understanding of the role of the RNAi genes in human fungal pathogens including C. neoformans. This SuperSeries is composed of the following subset Series: GSE21176: Molecular and Functional Characterization of the role of RNA silencing components in Cryptococcus neoformans [RNAi_Serotype A] GSE21177: Molecular and Functional Characterization of the role of RNA silencing components in Cryptococcus neoformans [RNAi_Serotype D] Refer to individual Series
2010-05-01 | E-GEOD-21178 | biostudies-arrayexpress
Project description:We examine the transcriptomic response of Cryptococcus neoformans to two different ecologically relevant nitrogen concentrations. Our data revealed that low nitrogen conditions modulate the expression of numerous virulence genes in C. neoformans. Among these were, CTR4 and CGP1, which showed highly significant modulation under low nitrogen conditions. Furthermore, data analysis revealed the upregulation of antifungal tolerance-related genes in low nitrogen conditions, including genes involved in ergosterol biosynthetic processes and cell wall integrity. Overall, our findings provide insight into the survival of C. neoformans in nitrogen-poor ecological niches and suggest that pre-adaptation to these conditions may influence the pathobiology of this yeast.
2021-01-23 | GSE165294 | GEO
Project description:Cryptococcus neoformans is the most common cause of fungal meningitis, with high mortality and morbidity. The reason for the frequent occurrence of Cryptococcus infection in the central nervous system (CNS) is poorly understood. In this study, we find that inositol plays an important role in the transversal of Cryptococcus across the blood-brain barrier (BBB) both in an in vitro human BBB model and in vivo animal models. The inositol stimulation of BBB crossing is dependent upon fungal inositol transporters. The upregulation of genes involved in the inositol catabolism pathway is evident in a microarray analysis. The expression of CPS1, a gene encoding the hyaluronic acid synthase in Cryptococcus, is also upregulated by the inositol treatment. The production of hyaluronic acid increased in cells treated with inositol, which leads to the enhanced binding ability of Cryptococcus cells to the human brain microvascular endothelial cells (HBMECs) constituting the BBB. Overall, our studies provide a mechanism for inositol-dependent Cryptococcus transversal of the BBB, supporting our hypothesis that host inositol utilization by the fungus contributes to Cryptococcus CNS infection.
2012-09-29 | GSE41211 | GEO