A unique cell wall synthetic response evoked by glucosamine determines pathogenicity-associated fungal cellular differentiation
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ABSTRACT:
PROVIDER: PRJNA610577 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11245055_1.fastq.gz | Fastqsanger.gz | |||
| SRR11245055_2.fastq.gz | Fastqsanger.gz | |||
| SRR11245056_1.fastq.gz | Fastqsanger.gz | |||
| SRR11245056_2.fastq.gz | Fastqsanger.gz | |||
| SRR11245057_1.fastq.gz | Fastqsanger.gz |
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Project description:The yeast-to-hypha transition is tightly associated with pathogenicity in many human pathogenic fungi, such as the model fungal pathogen Cryptococcus neoformans, which is responsible for approximately 180,000 deaths annually. In this pathogen, the yeast-to-hypha transition can be initiated by distinct stimuli: mating stimulation or glucosamine (GlcN), the monomer of cell wall chitosan. However, it remains poorly understood how the signal specificity for Cryptococcus morphological transition by disparate stimuli is ensured. Here, by integrating temporal expression signature analysis and phenome-based clustering evaluation, we demonstrate that GlcN specifically triggers a unique cellular response, which acts as a critical determinant underlying the activation of GlcN-induced filamentation (GIF). This cellular response is defined by an unusually hyperactive cell wall synthesis that is highly ATP-consuming. A novel cell surface protein Gis1 was identified as the indicator molecule for the GlcN-induced cell wall response. The Mpk1-directed cell wall pathway critically bridges global cell wall gene induction and intracellular ATP supply, ensuring the Gis1-dependent cell wall response and the stimulus specificity of GIF. We further reveal that the ability of Mpk1 to coordinate the cell wall response and GIF activation is conserved in different Cryptococcus pathogens. Phosphoproteomics-based profiling together with genetic and phenotypic analysis revealed that the Mpk1 kinase mediates the regulatory specificity of GIF through a coordinated downstream regulatory network centered on Skn7 and Crz1. Overall, our findings discover an unprecedented and conserved cell wall biosynthesis-dependent fungal differentiation commitment mechanism, which enables the signal specificity of pathogenicity-related dimorphism induced by GlcN in Cryptococcus pathogens.
2021-08-27 | GSE146435 | GEO
Project description:The yeast-to-hypha transition is tightly associated with pathogenicity in many human pathogenic fungi, such as the model fungal pathogen Cryptococcus neoformans, which is responsible for approximately 180,000 deaths annually. In this pathogen, the yeast-to-hypha transition can be initiated by distinct stimuli: mating stimulation or glucosamine (GlcN), the monomer of cell wall chitosan. However, it remains poorly understood how the signal specificity for Cryptococcus morphological transition by disparate stimuli is ensured. Here, by integrating temporal expression signature analysis and phenome-based clustering evaluation, we demonstrate that GlcN specifically triggers a unique cellular response, which acts as a critical determinant underlying the activation of GlcN-induced filamentation (GIF). This cellular response is defined by an unusually hyperactive cell wall synthesis that is highly ATP-consuming. A novel cell surface protein Gis1 was identified as the indicator molecule for the GlcN-induced cell wall response. The Mpk1-directed cell wall pathway critically bridges global cell wall gene induction and intracellular ATP supply, ensuring the Gis1-dependent cell wall response and the stimulus specificity of GIF. We further reveal that the ability of Mpk1 to coordinate the cell wall response and GIF activation is conserved in different Cryptococcus pathogens. Phosphoproteomics-based profiling together with genetic and phenotypic analysis revealed that the Mpk1 kinase mediates the regulatory specificity of GIF through a coordinated downstream regulatory network centered on Skn7 and Crz1. Overall, our findings discover an unprecedented and conserved cell wall biosynthesis-dependent fungal differentiation commitment mechanism, which enables the signal specificity of pathogenicity-related dimorphism induced by GlcN in Cryptococcus pathogens.
2021-09-15 | PXD018015 | Pride
Project description:The yeast-to-hypha transition is tightly associated with pathogenicity in many human pathogenic fungi, such as the model fungal pathogen Cryptococcus neoformans, which is responsible for approximately 180,000 deaths annually. In this pathogen, the yeast-to-hypha transition can be initiated by distinct stimuli: mating stimulation or glucosamine (GlcN), the monomer of cell wall chitosan. However, it remains poorly understood how the signal specificity for Cryptococcus morphological transition by disparate stimuli is ensured. Here, by integrating temporal expression signature analysis and phenome-based clustering evaluation, we demonstrate that GlcN specifically triggers a unique cellular response, which acts as a critical determinant underlying the activation of GlcN-induced filamentation (GIF). This cellular response is defined by an unusually hyperactive cell wall synthesis that is highly ATP-consuming. A novel cell surface protein Gis1 was identified as the indicator molecule for the GlcN-induced cell wall response. The Mpk1-directed cell wall pathway critically bridges global cell wall gene induction and intracellular ATP supply, ensuring the Gis1-dependent cell wall response and the stimulus specificity of GIF. We further reveal that the ability of Mpk1 to coordinate the cell wall response and GIF activation is conserved in different Cryptococcus pathogens. Phosphoproteomics-based profiling together with genetic and phenotypic analysis revealed that the Mpk1 kinase mediates the regulatory specificity of GIF through a coordinated downstream regulatory network centered on Skn7 and Crz1. Overall, our findings discover an unprecedented and conserved cell wall biosynthesis-dependent fungal differentiation commitment mechanism, which enables the signal specificity of pathogenicity-related dimorphism induced by GlcN in Cryptococcus pathogens.
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Project description:We did transcription profiling on the effect of glucosamine in Saccharomyces cerevisiae using Research Genetics strains BY4741 (wild type) and 5251 (fks1). Yeast cells exposed to glucosamine in YPD growth medium show a significant increase in chitin content in the lateral cell wall. Likewise, cell wall stress caused by a gene deletion e.g., fks1 also results in elevated chitin. By comparing our data for fks1 with those from the literature we confirmed a strong induction of genes responsive to cell wall integrity, environmental stress as well as genes involved in cell signaling. Wild type cells treated with 15 mM glucosamine for 2 hours did not show any significant change in their transcription profile although the chitin level doubled during this time. For cells continuously exposed to glucosamine (steady state) there was a moderate transcription response, 105 genes showed a two-fold or higher change. The largest groups of up-regulated genes were those involved in mating, sporulation and cell cycle arrest. The largest group of down-regulated genes pertained to mitochondrial respiration. There was little overlap between those genes that have altered transcription from glucosamine treatment and those responsive to the fks1 mutation. Keywords = saccharomyces chitin glucosamine Keywords: parallel sample
2003-05-30 | GSE441 | GEO
Project description:We did transcription profiling on the effect of glucosamine in Saccharomyces cerevisiae using Research Genetics strains BY4741 (wild type) and 5251 (fks1). Yeast cells exposed to glucosamine in YPD growth medium show a significant increase in chitin content in the lateral cell wall. Likewise, cell wall stress caused by a gene deletion e.g., fks1 also results in elevated chitin. By comparing our data for fks1 with those from the literature we confirmed a strong induction of genes responsive to cell wall integrity, environmental stress as well as genes involved in cell signaling. Wild type cells treated with 15 mM glucosamine for 2 hours did not show any significant change in their transcription profile although the chitin level doubled during this time. For cells continuously exposed to glucosamine (steady state) there was a moderate transcription response, 105 genes showed a two-fold or higher change. The largest groups of up-regulated genes were those involved in mating, sporulation and cell cycle arrest. The largest group of down-regulated genes pertained to mitochondrial respiration. There was little overlap between those genes that have altered transcription from glucosamine treatment and those responsive to the fks1 mutation.
2007-07-07 | E-GEOD-441 | biostudies-arrayexpress
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Project description:Define regulated genes upon 24 hours of glucosamine treatment in KMH2 and Ramos
2014-08-18 | GSE49185 | GEO
Project description:Glucosamine proved to be a potent, broad-spectrum inhibitor of IL-1beta. Of the 2,813 genes whose transcription was altered by IL-1beta stimulation (p<0.0001), glucosamine significantly blocked the response in 2,055 (~73%). Glucosamine fully protected the chondrocytes from IL-1-induced expression of inflammatory cytokines, chemokines and growth factors as well as proteins involved in PGE2 and NO synthesis. It also blocked the IL-1-induced expression of matrix specific proteases such as MMPs -3,-9,-10,-12 and ADAMTS-1. Experiment Overall Design: Articular cartilage was isolated from the femoral heads of male Wistar rats under aseptic conditions. Chondrocytes were obtained by sequential digestion of the cartilage with pronase and type II collagenase. After filtration to remove tissue debris, the cells were cultured in 75-cm2 flasks in complete Dulbeccoâs Modified Eagle Medium (DMEM; supplemented with 10% fetal bovine serum and 1% penicillin-streptomycin at 37°C in a humidified atmosphere containing 5% CO2. Experiments were subsequently performed with second-passage cultures whereby the cells from the large cultures were trypsinized, pooled and seeded into twenty 25 cm2 flasks. These were then divided into 4 treatment groups to evaluate the effects of glucosamine and IL-1 on global transcription patterns.To the culture medium in half of the flasks, glucosamine, HCl was added to a final concentration of 20 mM. Six hours later, IL-1beta was added at 10 ng/ml to 5 of the flasks receiving glucosamine and to 5 of the untreated flasks. Fourteen hours post IL-1beta stimulation, total RNA was isolated individually from the respective cultures and microarray experiments processed.
2009-04-23 | E-GEOD-6119 | biostudies-arrayexpress
Project description:Glucosamine proved to be a potent, broad-spectrum inhibitor of IL-1beta. Of the 2,813 genes whose transcription was altered by IL-1beta stimulation (p<0.0001), glucosamine significantly blocked the response in 2,055 (~73%). Glucosamine fully protected the chondrocytes from IL-1-induced expression of inflammatory cytokines, chemokines and growth factors as well as proteins involved in PGE2 and NO synthesis. It also blocked the IL-1-induced expression of matrix specific proteases such as MMPs -3,-9,-10,-12 and ADAMTS-1. Keywords: treatment response
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