Cryptococcus neoformans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA184866 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR641950.fastq.gz | Fastqsanger.gz | |||
| SRR641951.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
Similar Datasets
Project description:WT vs rim101 mutant gene expression under capsule inducing conditions
| PRJNA130327 | ENA
Project description:Cryptococcus neoformans is an invasive human fungal pathogen, which causes pneumonia and meningoencephalitis in both healthy and immunodeficient individuals, resulting 181,100 deaths each year. Studies have demonstrated that copper detoxification machineries play critical functions in modulating C. neoformans fitness and pathogenicity in the host lung tissue. Pulmonary C. neoformans infection provokes the generation of toxic copper bombardment, which in return activate detoxification process in fungal cells. However, the molecular mechanism on how Cu inhibits C. neoformans in proliferation remains unclear. Here, using Cu detoxification gene knockout strains we demonstrated that exogenous Cu ions inhibit cell growth of the metallothionein mutant, which was significantly rescue when supplementing with the ROS scavenger, N-acetylcysteine. To future characterize the molecular mechanism of C. neoformans response to Cu toxicity, we employ iTRAQ with LC-MS/MS analysis, in the presence of exogenous Cu or NAC. Our data showed that an increased Cu level repressed expression of factors involved in protein translation but activates expression of important players in ubiquitin-degradation process. We proposed that the downregulation of protein synthesis and the upregulation of protein degradation were the main strategy of Cu toxicity. The metallothionein mutant showed a higher ubiquitination level under Cu treatment. In addition, MG132 could partially restore the Cu toxicity effect on metallothionein mutant. These results shed new light on the Cu antifungal mechanisms from proteomic profile.
2021-02-09 | PXD024098 |
Project description:Cryptococcus neoformans gene expression in minimal media of wild type (WT) and all1all2Δ mutant cells
| PRJNA299667 | ENA
Project description:Cryptococcus neoformans gene expression in minimal media of wild type (WT) and ALL2 mutant (all2Δ) cells
| PRJNA299668 | ENA
Project description:Cryptococcus neoformans gene expression in YPD and Minimal Media of Wild type (WT) and ALL1 mutant cells
| PRJNA195610 | ENA
Project description:Analysis of the transcriptional response of C. neoformans WT, cir1 mutant, hap3 mutant and hapX mutant to different iron sources.
2011-04-13 | GSE22988 | GEO
Project description:The core virulence kinase Bud32, which is critical for lung and brain infections, influences the production of major virulence factors in Cryptococcus neoformans, including capsule formation, melanin production, and growth at 37°C. This study explores the role of Bud32 in regulation of iron homeostasis in C. neoformans. Bud32 was required for growth under iron limiting condition. Loss of Bud32 resulted in significant alterations in the expression of proteins related to iron binding and iron-sulfur cluster assembly. Moreover, metabolic profiling identified 696 metabolites that were up-regulated and 480 that were down-regulated in the bud32 deletion mutant, highlighting the significant impact of Bud32 loss on intracellular metabolite levels. In particular, the levels of biliverdin, which is primarily derived from heme, showed a significant decrease in the absence of Bud32. Furthermore, Bud32 has been demonstrated to modulate iron-sulfur cluster assembly, likely influencing the interaction between the iron-sulfur binding protein Grx4 and the iron regulatory factors Cir1 and HapX. Phosphorylation analysis revealed that the deletion of Bud32 caused widespread changes in the phosphorylation status of various proteins, including the iron regulatory factors Cir1 and Rim101. These findings indicate that the Bud32 kinase plays a vital role in regulating iron homeostasis in C. neoformans.
2025-07-23 | PXD056845 | Pride
Project description:The core virulence kinase Bud32, which is critical for lung and brain infections, influences the production of major virulence factors in Cryptococcus neoformans, including capsule formation, melanin production, and growth at 37°C. This study explores the role of Bud32 in regulation of iron homeostasis in C. neoformans. Bud32 was required for growth under iron limiting condition. Loss of Bud32 resulted in significant alterations in the expression of proteins related to iron binding and iron-sulfur cluster assembly. Moreover, metabolic profiling identified 696 metabolites that were up-regulated and 480 that were down-regulated in the bud32 deletion mutant, highlighting the significant impact of Bud32 loss on intracellular metabolite levels. In particular, the levels of biliverdin, which is primarily derived from heme, showed a significant decrease in the absence of Bud32. Furthermore, Bud32 has been demonstrated to modulate iron-sulfur cluster assembly, likely influencing the interaction between the iron-sulfur binding protein Grx4 and the iron regulatory factors Cir1 and HapX. Phosphorylation analysis revealed that the deletion of Bud32 caused widespread changes in the phosphorylation status of various proteins, including the iron regulatory factors Cir1 and Rim101. These findings indicate that the Bud32 kinase plays a vital role in regulating iron homeostasis in C. neoformans.
2025-07-23 | PXD056847 | Pride
Project description:Purpose: To examine the comparative transcriptional profiles of WT and rim101 mutant cells in host-mimicking in vitro conditions to determine genes that are responsible for the increased virulence of the rim101 strain. The rim101 mutant is able to trigger an overactive inflammatory response, presumably by exposing an antigenic trigger. Using transcriptional profiling, we determined that many genes involved in cell wall processes were differentially transcribed between the wild type and the mutant strain.
2013-02-02 | GSE43189 | GEO
Project description:To investigate the pleiotropic roles of Lkh1 in stress response and virulence, we constructed lkh1∆ mutant strains. In this study, we found that Tor1 was an upstream regulator of Lkh1 in C. neoformans. We then performed gene expression profiling analysis to elucidate signaling circuitry downstream of CnLkh1 in the TOR1-Lkh1 pathway using data obtained from RNA seq of 2 different strains (WT of lkh1∆ mutant) with or without rapamycin treatment.
2023-12-31 | GSE233612 | GEO