Cryptococcus neoformans
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PROVIDER: PRJNA127769 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Understanding the iron-responsive regulatory networks in Cryptococcus neoformans. Methods: The transcriptome profiles of the wild-type, cir1 mutant and hapX mutant were generated by RNA-seq using Illumina Hiseq, in triplicate. The transcriptome profiles of each mutant was compared with that of the wild-type strain. Results: The iron-responsive transcription factors, Cir1 and HapX, are major regulators for iron acquisition and metabolism in C. neoformans.
2020-02-16 | GSE126313 | GEO
Project description:The opportunistic pathogen Cryptococcus neoformans causes fungal meningoencephalitis in immunocompromised individuals. In previous studies, we found that the Hap complex in this pathogen represses genes encoding mitochondrial respiratory functions and TCA cycle components under low-iron conditions. The orthologous Hap2/3/4/5 complex in Saccharomyces cerevisiae exerts a regulatory influence on mitochondrial functions and Hap4 is subject to glucose repression via the carbon catabolite repressor Mig1. In this study, we explored the regulatory link between a candidate ortholog of the Mig1 protein and the HapX component of the Hap complex in C. neoformans. This analysis revealed repression of MIG1 by HapX and activation of HAPX by Mig1 in low iron conditions, and Mig1 regulation of mitochondrial functions including respiration, tolerance for reactive oxygen species, and expression of genes for iron-consuming and iron-acquisition functions. Consistent with these regulatory functions, a mig1Î mutant had impaired growth on inhibitors of mitochondrial respiration and ROS inducers. Furthermore, deletion of MIG1 provoked a dysregulation in nutrient sensing via the TOR pathway and impacted the pathway for cell wall remodeling. Importantly, loss of Mig1 increased susceptibility to fluconazole thus further establishing a link between azole antifungal drugs and mitochondrial function. Mig1 and HapX were also required together for survival in macrophages, but Mig1 alone had a minimal impact on virulence in mice. Overall, these studies provide novel insights into a HapX/Mig1 regulatory network and reinforce an association between mitochondrial dysfunction and drug susceptibility that may provide new targets for the development of antifungal drugs. In this study, transcription profiles of WT and mig1D mutant strains of Cryptococcus neoformans were compared in a dye-swap experiment following 6hr exposure to Low Iron Medium (LIM) or LIM + 100mM FeCl3.
2015-12-17 | E-GEOD-76063 | biostudies-arrayexpress
Project description:Purpose: Defining the regulatory role of the transcription factors, Cir1 and HapX, in C. neoformans. Methods: Chromatin immunoprecipitation followed by high-throughput sequencing was performed using chromatin immunoprecipitated DNA from the strains Cir1-Flag and HapX-Flag grown in low- and high-iron condition. Results: Cir1 and HapX bind to the promoter region of the genes involved in iron acquisition and metabolism in C. neoformans.
2020-02-16 | GSE126312 | GEO
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 opportunistic pathogen Cryptococcus neoformans causes fungal meningoencephalitis in immunocompromised individuals. In previous studies, we found that the Hap complex in this pathogen represses genes encoding mitochondrial respiratory functions and TCA cycle components under low-iron conditions. The orthologous Hap2/3/4/5 complex in Saccharomyces cerevisiae exerts a regulatory influence on mitochondrial functions and Hap4 is subject to glucose repression via the carbon catabolite repressor Mig1. In this study, we explored the regulatory link between a candidate ortholog of the Mig1 protein and the HapX component of the Hap complex in C. neoformans. This analysis revealed repression of MIG1 by HapX and activation of HAPX by Mig1 in low iron conditions, and Mig1 regulation of mitochondrial functions including respiration, tolerance for reactive oxygen species, and expression of genes for iron-consuming and iron-acquisition functions. Consistent with these regulatory functions, a mig1Δ mutant had impaired growth on inhibitors of mitochondrial respiration and ROS inducers. Furthermore, deletion of MIG1 provoked a dysregulation in nutrient sensing via the TOR pathway and impacted the pathway for cell wall remodeling. Importantly, loss of Mig1 increased susceptibility to fluconazole thus further establishing a link between azole antifungal drugs and mitochondrial function. Mig1 and HapX were also required together for survival in macrophages, but Mig1 alone had a minimal impact on virulence in mice. Overall, these studies provide novel insights into a HapX/Mig1 regulatory network and reinforce an association between mitochondrial dysfunction and drug susceptibility that may provide new targets for the development of antifungal drugs.
2015-12-17 | GSE76063 | 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:Analysis of the transcriptional response of C. neoformans WT, cir1 mutant, hap3 mutant and hapX mutant to different iron sources. The following experimental design was adopted for the study. Within each strain, each treatment pair (low-iron, +FeCl3, +Transferrin and +Hemin; 6 pairs) were hybridized to an array; and within each treatment, each strain (WT, hap3, hapX and cir1, 6 pairs) were hybridized to an array for a total of 48 microarrays. Each strain/treatment combination was labeled an equal number of times with Cy3 and Cy5 to ensure dye balance
2011-04-13 | E-GEOD-22988 | 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:Light is a universal environmental signal perceived by many organisms, including the fungi in which light regulates both common and unique biological processes depending on the species. We conducted a whole-genome microarray analysis on the basidiomycete fungus Cryptococcus neoformans to identify light-regulated genes.
2010-04-23 | GSE21484 | GEO