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A new regulator in the crossroads of oxidative stress resistance and virulence in Candida glabrata: the transcription factor CgTog1

ABSTRACT: A new regulator in the crossroads of oxidative stress resistance and virulence in Candida glabrata: the transcription factor CgTog1

PROVIDER: PRJNA623751 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11509872_1.fastq.gz	Fastqsanger.gz
	SRR11509872_2.fastq.gz	Fastqsanger.gz
	SRR11509873_1.fastq.gz	Fastqsanger.gz
	SRR11509873_2.fastq.gz	Fastqsanger.gz
	SRR11509874_1.fastq.gz	Fastqsanger.gz

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Candida glabrata oxidative stress

Project description:Investigating the oxidative stress response: Candida glabrata strains were stressed with hydrogen peroxide and menadione (causing oxygen radicals) to induce the oxidative stress regulon, which is thought to be upregulated during the oxidative burst inside of phagocytic cells.

2011-01-01 | E-MEXP-2915 | biostudies-arrayexpress

Histone Acetylation Regulator Gcn5 Mediates Drug Resistance and Virulence of Candida glabrata

Project description:Histone Acetylation Regulator Gcn5 Mediates Drug Resistance and Virulence of Candida glabrata

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Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata

Project description:This SuperSeries is composed of the following subset Series: GSE23827: Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata (part 1) GSE23828: Contribution of CgPDR1-regulated genes in enhanced virulence of azole-resistant Candida glabrata (part 2) Refer to individual Series

2010-12-31 | E-GEOD-23829 | biostudies-arrayexpress

A new regulator in the crossroads of oxidative stress resistance and virulence in Candida glabrata: the transcription factor CgTog1

Project description:The goals of this study are to compare C. glabrata transcriptome profiling (RNA-seq) upon exposure to hydrogen peroxide in order to assess the correspondent response. The role of the transcription factor Tog1 is clarified through comparison of the transcrptome profiles of WT and Tog1 mutant cells. mRNA profiles of WT and ∆tog1 were generated by deep sequencing, in duplicate, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed with TopHat followed by HTSeq. RNA-seq data allowed to identify genes whose expression is regulated by the Tog1 transcription factor (147 positively regulated and 112 negatively regulated) with a log2fold change ≥0.5 and p value <0.05. The transcriptomics data was then used to guide further work to detail the function of Tog1.

2020-04-09 | GSE148288 | GEO

Histone Acetylation Regulator Gcn5 Mediates Drug Resistance and Virulence of Candida glabrata

Project description:This study explored the transcriptional change of Candida glabrata cells due to GCN5 deletion. We also compared the transcriptional responses to fluconazole and micafungin in WT and gcndelta cells relative to respective no drug controls.

2022-01-28 | GSE194310 | GEO

Loss of mitochondrial functions in Candida glabrata results in enhanced virulence in mice

Project description:Two C. glabrata related isolates recovered from the same patient undergoing azole therapy were characterized. The first isolate, BPY40, is azole-susceptibleand the second, BPY41, is azole-resistant. To determine whether the petite mutation conferred a selective advantage during host infection, the virulence of BPY40 and BPY41 was assessed in mice. Surprisingly, the petite mutant, even if showing in vitro growth deficiency as compared to BPY40, was more virulent than BPY40 both in intravenous and vaginal murine infection models. The increased virulence of the petite mutant correlated with a drastic gain of fitness in mice as compared to its parental isolate. Genome-wide changes in gene expression driven by the petite mutation were analyzed by microarrays. Enrichment of specific biological processes (oxido-reductive metabolism, stress response) was observed in BPY41, all consistent with mitochondrial dysfunction. Finally, some genes involved in cell wall genome-wide changes in gene expression driven by the petite mutation were analyzed by microarrays. Enrichment of specific biological processes (oxido-reductive metabolism, stress response) was observed in BPY41, all consistent with mitochondrial dysfunction. Gene expression was measured in 2 related C. glabrata clinical isolates (BPY40 and BPY41). The one-color system was used . 3 independent experiments were performed using 3 biological replicate for each strain.

2010-12-31 | E-GEOD-23826 | biostudies-arrayexpress

An AraC/XylS Family Transcriptional Regulator Modulates the Oxidative Stress Response of Francisella tularensis

Project description:Francisella tularensis is a Gram-negative bacterium that causes a fatal human disease known as tularemia. The Centers for Disease Control have classified F. tularensis as Category A Tier-1 Select Agent. The virulence mechanisms of Francisella are not entirely understood. Francisella possesses very few transcription regulators, and most of these regulate the expression of genes involved in intracellular survival and virulence. The F. tularensis genome sequence analysis reveals an AraC (FTL_0689) transcriptional regulator homologous to the AraC/XylS family of transcriptional regulators. In Gram-negative bacteria, AraC activates genes required for L-arabinose utilization and catabolism. The role of the FTL_0689 regulator in F. tularensis is not known. In this study, we characterized the role of FTL_0689 in gene regulation of F. tularensis and investigated its contribution to intracellular survival and virulence. The results demonstrate that FTL_0689 in Francisella is not required for L-arabinose utilization. Instead, FTL_0689 specifically regulates the expression of the oxidative and global stress response, virulence, metabolism, and other key pathways genes required by Francisella when exposed to oxidative stress. The FTL_0689 mutant is attenuated for intramacrophage growth, and mice infected with the FTL_0689 mutant survive better than wild-type F. tularensis LVS infected mice. Based on the deletion mutant phenotype, FTL_0689 was termed osrR (oxidative stress response regulator). Altogether, this study elucidates the role of the osrR transcriptional regulator in tularemia pathogenesis.

2021-10-13 | GSE183001 | GEO

Loss of mitochondrial functions in Candida glabrata results in enhanced virulence in mice

2010-12-31 | GSE23826 | GEO

Characterization of PlcRa, a new PlcR-like regulator involved in oxidative stress response and cysteine metabolism during early stationary phase in Bacillus cereus

Project description:PlcR, the major virulence transcriptional regulator in the Bacillus cereus group belongs to the RNPP quorum sensor family and is activated through interaction with the secreted heptapeptide PapR7 used as a signalling molecule. We identified using modeling analysis a structural homologue of PlcR, PlcRa, in B. cereus. Whole-genome comparative microarrays identified 119 genes (threshold >3) differentially expressed at the onset of stationary phase in a plcRa mutant. phBC6A51 and phBC6A52 prophage genes were up-expressed in a plcRa mutant. Genes involved in oxidative stress response and in cysteine metabolism, including genes which belong to the CymR regulon, were down-regulated in a plcRa mutant. Accordingly, deletion of plcRa resulted in increased sensitivity to hydrogen peroxide and disulfide induced stresses. We also characterized a major target of PlcRa, the (BC2444) abrB2 gene, encoding a putative regulator belonging to AbrB family. PlcRa controlled CymR-regulated genes through AbrB2 and deletion of abrB2 gene resulted in increased sensitivity to hydrogen peroxide and disulfide induced stresses. In conclusion, we identified a new early stationary transcriptional regulator specific to B. cereus group members involved in oxidative stress response and CymR regulon activation. Two different comparisons were performed (both in biological duplo and Cy5-Cy3 dye-swapped) using 2 different time points: (1) B.cereus WT versus B. cereus plcRa overexpression strain at T1 (one hour after the onset of stationary phase) and T2 (two hours after the onset of stationary phase). (2) B.cereus WT versus B.cereus plcRa deletion strain at T1 and T2

2012-12-14 | E-GEOD-30514 | biostudies-arrayexpress

The Candida glabrata transcription factor Stb5p is a negative regulator of ATP-binding cassette transporters

Project description:The opportunistic yeast pathogen Candida glabrata is recognized for its ability to acquire resistance during prolonged treatment with azole antifungals. Resistance to azoles is largely mediated by the transcription factor PDR1, resulting in the upregulation of ATP-binding cassette (ABC) transporter proteins and drug efflux. Studies in the related yeast Saccharomyces cerevisiae have shown Pdr1p forms a heterodimer with another transcription factor, Stb5p. In C. glabrata the ORF designated CAGL0I02552g has 38.8% amino acid identity with STB5 (YHR178w), and shares an N-terminal Zn2Cys6 binuclear cluster domain and a fungal specific transcriptional factor domain, prompting us to test for homologous function and a possible role in azole resistance. Complementation of deltayhr178w (stb5) with CAGL0I02552g resolved the increased sensitivity to cold, hydrogen peroxide and caffeine of the mutant, for which reason we designated CAGl0I02552g as CgSTB5. Overexpression of CgSTB5 in C. glabrata repressed azole resistance, whereas deletion of CgSTB5 increased resistance, both by a mechanism independent of CgPDR1. Expression analysis found that CgSTB5 shares many of the same transcriptional targets as CgPDR1 but, unlike the later, is a negative regulator of pleiotropic drug resistance, including the ABC transporter genes CDR1,PDH1, and YOR1.

2013-03-11 | GSE37071 | GEO

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