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General retardation of mRNA degradation caused by speB 5’ UTR partial deletion in Streptococcus pyogenes

ABSTRACT: The speB gene of Streptococcus pyogenes has a long 5' UTR with unknown functions. Preliminary studies showed that the partial mutation of this region led to altered expression patterns of the speB gene and ropB, its upstream gene. In this study, we used microarray to examine the effect of speB 5' UTR mutation on the S. pyogenes transcriptome.

ORGANISM(S): Streptococcus pyogenes Streptococcus pyogenes NZ131

PROVIDER: GSE72838 | GEO | 2015/09/10

SECONDARY ACCESSION(S): PRJNA295190

REPOSITORIES: GEO

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General retardation of mRNA degradation caused by speB 5’ UTR partial deletion in Streptococcus pyogenes

Project description:The speB gene of Streptococcus pyogenes has a long 5' UTR with unknown functions. Preliminary studies showed that the partial mutation of this region led to altered expression patterns of the speB gene and ropB, its upstream gene. In this study, we used microarray to examine the effect of speB 5' UTR mutation on the S. pyogenes transcriptome. The speB ORF and a large portion of the speB 5’ UTR (-1 to -527 from ATG) was replaced with an erythromycin resistant cassette gene (ermAM) to generate a ΔIG mutant. Transcriptome profiles of the wild-type (WT) and ΔIG mutant in the mid-exponential phase and early stationary phase (ST) were examined with microarray analysis.

2015-09-10 | E-GEOD-72838 | biostudies-arrayexpress

Streptococcus pyogenes

Project description:General retardation of mRNA degradation caused by speB 5’ UTR partial deletion in Streptococcus pyogenes

| PRJNA295190 | ENA

Neutrophil-derived reactive agents induce a transient SpeB negative phenotype in Streptococcus pyogenes

Project description:Streptococcus pyogenes (group A streptococci; GAS) is the main causative pathogen of monomicrobial necrotizing soft tissue infections (NSTIs). To resist immuno-clearance, GAS adapt their genetic information and/or phenotype to the surrounding environment. Hyper-virulent streptococcal pyrogenic exotoxin B (SpeB) negative variants caused by covRS mutations are enriched during infection. A key driving force for this process is the bacterial Sda1 DNase. Here, we identify another strategy resulting in SpeB-negative variants, namely reversible abrogation of SpeB secretion triggered by neutrophil effector molecules. Analysis of NSTI patient tissue biopsies revealed that tissue inflammation, neutrophil influx, and degranulation positively correlate with increasing frequency of SpeB-negative GAS clones. Using single colony proteomics, we show that GAS isolated directly from tissue express but do not secrete SpeB. Once the tissue pressure is lifted, GAS regain SpeB secreting function. Neutrophils were identified as the main immune cells responsible for the observed phenotype. Subsequent analyses identified hydrogen peroxide and hypochlorous acid as reactive agents driving this phenotypic GAS adaptation to the tissue environment. SpeB-negative GAS show improved survival within neutrophils and induce increased degranulation. Our findings provide new information about GAS fitness and heterogeneity in the soft tissue milieu and provide new potential targets for therapeutic intervention in NSTIs.

2023-10-24 | PXD040160 | Pride

Comparison of gene expression in the GAS M1T1 strain 5448, wild-type vs pepO mutant

Project description:Manuscript title: The endopeptidase PepO regulates the SpeB cysteine protease and is essential for the virulence of invasive M1T1 Streptococcus pyogenes. The study investigates the effect of pepO mutation on global gene expression in GAS M1T1 strain 5448.

2018-01-05 | GSE108748 | GEO

Gene expression of GidA mutant Streptococcus pyogenes

Project description:In Streptococcus pyogenes, mutation of GidA results in avirulence despite the same growth rate as the wild type. To understand the basis of this effect, global transcription profiling was conducted. Keywords: Wild type vs. GidA mutant Streptococcus pyogenes

2008-01-10 | GSE9678 | GEO

Insert in CovS Gene Distinguishes a Pharyngeal and a Blood Isolate of Streptococcus pyogenes Found in the Same Individual.

Project description:Expression of the extensive arsenal of virulence factors by Streptococcus pyogenes are controlled by many regulators, of which covR/S is one of the best characterized and can influence ~15% of the genome. Animal models have established that mutants of CovR/S arise spontaneously in vivo resulting in highly invasive organisms. We analyzed a pharyngeal and a blood isolate of S. pyogenes recovered from the same individual 13 days apart. The two isolates varied in many phenotypic properties including speB production, which were reflected in transcriptome analyses. Pulsed field gel electrophoresis, multilocus sequence typing, and partial sequencing of some key genes failed to show any differences except for an 11-base insert in the covS gene in the blood isolate. These results showing that pharyngeal and blood isolates from a single individual which differ by a simple insertion, provide evidence for the model that regulatory gene mutations allow S. pyogenes to invade different niches in the body. A chip study using total RNA recovered from two separate wild-type cultures of group A Streptococcus, Streptococcus pyogenes UH322 and UH328. Each chip measures the expression level of 1865 genes replicated twice from 7 fully sequenced strains of Streptococcus pyogenes (M1_GAS NC_002737; MGAS10394 NC_006086; MGAS315 NC_004070; MGAS5005 NC_007297; MGAS6180 NC_007296; MGAS8232 NC_003485; SSI-1 NC_004606 with fourteen 24-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.

2010-05-01 | E-GEOD-21316 | biostudies-arrayexpress

Insert in CovS Gene Distinguishes a Pharyngeal and a Blood Isolate of Streptococcus pyogenes Found in the Same Individual.

2010-05-01 | GSE21316 | GEO

Transcriptome study of the covS-regulation of a Group A Streptococcus pyogenes M23ND

Project description:We investigated the covS-regulation of S. pyogenes in a hypervirulent M23 strain using RNA-sequencing. The differential gene expression comparison between the covS- mutant and isogenic wild type covS+ identified altered expression of 349 (18%) genes, including a broad spectrum of virulence genes and diverse metabolic genes. The data showed that the strain achieved hypervirulence by enhancing the expression of genes responsible for invasiveness and antiphagocytosis (i.e., hasABC), by abrogating the expression of toxic genes (i.e., speB), and by compromising gene products with dispensable functions (i.e., sfb1). Meanwhile, we found that covS also regulated diverse kinds of metabolic genes that maximized nutrient utilization and energy metabolism during growth and dissemination. From constructing a genome-scale metabolic model, we identified fourteen non-redundant metabolic gene modules, which constitute unique sources for specific nutrients. These genes were probably essential for pathogen growth and virulence. In general, this study provided quantitative transcriptomic signatures of the covS regulation in a hypervirulent S. pyogenes strain and addressed major aspects of the covS-modulated virulent mechanisms. Examination of expression profiling of covS- mutant strain and isogenic wild type covS+ at different growth stages.

2015-08-05 | E-GEOD-67533 | biostudies-arrayexpress

Wild type versus PerR mutant Streptococcus pyogenes

Project description:In Streptococcus pyogenes, mutation of the peroxide sensor PerR results in avirulence despite producing hyper-resistance to peroxide stress. To understand the basis of this effect, global transcription profiling was conducted. Keywords: Study of the regulation of gene expression by PerR

2007-04-01 | GSE6384 | GEO

Transcriptome study of the covS-regulation of a Group A Streptococcus pyogenes M23ND

2015-08-05 | GSE67533 | GEO

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