Streptococcus pyogenes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA147469 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:GAS M6 serotype, wild-type vs covR mutant
| PRJNA93501 | ENA
Project description:Two covR mutant derivatives of parental strain MGAS2221 were recovered from mice experimentally infected with MGAS2221 and shown to differ in terms of the number and concentration of secreted proteins. One of the covR mutant strains had a secretion phenotype identical to a covS mutant strain, while the other had a secretion phenotype identical to a constructed covR mutant strain. To further investigate the potential differences between the two covR mutant strains we performed expression microarray analysis. Single cultures of each of the four GAS strains tested were grown in THY broth to early exponential phase (O.D. 0.2). Two volumes of RNA protect were added, the samples incubated at room temperature for 5 minutes, and the bacteria collected through centrifugation. Total RNA was isolated via a mechaniscal disruption method, converted to cDNA, fragmented, labeled, and hybridized to our Affymetrix microarray. Estimates of gene expression were calculated using GCOS software v1.4. Data represent probes for serotype M1.
2009-06-05 | E-GEOD-16436 | biostudies-arrayexpress
Project description:GAS gene expression from mouse-passaged and clinical GAS strains
| PRJNA94149 | ENA
Project description:GAS gene expression from clinical samples
| PRJNA94151 | ENA
Project description:Transcriptional profiling of Streptococcus pyogenes MGAS5005 cells comparing control untreated GAS cells with GAS cells exposed to 4uM heme for 1.5 h
2014-09-16 | GSE61415 | GEO
Project description:The control of virulence two-component gene regulatory system (CovRS) is critical to the pathogenesis of many medically important streptococci. In emm1 group A streptococci (GAS), CovR directly binds the promoters of numerous GAS virulence factor encoding genes. Elimination of CovS phosphatase activity increases CovR phosphorylation (CovR~P) levels and abrogates GAS virulence. Given the emm type-specific diversity of CovRS function, herein we used ChIP-seq to define global CovR DNA occupancy in the wild-type emm3 strain MGAS10870 (medium CovR~P) and its CovS phosphatase-negative derivative 10870-CovS-T284A (high CovR~P). In the wild-type emm3 strain, 89% of the previously identified emm1 CovR binding sites present in the emm3 genome were also enriched; additionally, we ascertained unique CovR binding, primarily to genes in mobile genetic elements and other sites of inter-strain chromosomal differences. Elimination of phosphatase activity specifically increased CovR occupancy at the promoters of a broad array of CovR repressed virulence factor encoding genes, including those encoding the key GAS regulator Mga and M protein. However, a limited number of promoters had augmented enrichment at low CovR~P levels. Differential motif searches using sequences enriched at high vs. low CovR~P levels revealed two distinct binding patterns. At high CovR~P, a pseudo-palindromic AT-rich consensus sequence consistent with CovR binding as a dimer was determined. Conversely, sequences specifically enriched at low CovR~P contained isolated “ATTARA” motifs suggesting an interaction with a monomer. These data extend understanding of global CovR DNA occupancy beyond emm1 GAS and provide a mechanism for previous observations regarding hypovirulence induced by CovS phosphatase abrogation.
2023-05-31 | GSE230870 | GEO
Project description:Effect of CovR phosphorylation on the transcriptome of streptococcus pyogenes M1 M3 Fall 2018
| PRJNA493791 | ENA
Project description:The mechanisms by which bacteria sense the host environment and alter gene expression are poorly understood. LiaFSR is a gene regulatory system unique to Gram-positive bacteria including group A Streptococcus (GAS) and responds to cell envelope stress. We previously showed that LiaF acts as an inhibitor to LiaFSR activation in GAS. To better understand gene regulation associated with LiaFSR activation, we performed RNA-sequencing on isogenic deletion mutants fixed in a LiaFSR “always on” (DliaF) or “always off” (DliaR) state. Transcriptome analyses of DliaF and DliaR in GAS showed near perfect inverse correlation including the gene encoding the global transcriptional regulator SpxA2. In addition, mutant transcriptomes included genes encoding multiple virulence factors and showed substantial overlap with the CovRS regulon. Chromatin immunoprecipitation quantitative PCR demonstrated direct spxA2 gene regulation following activation of the response regulator, LiaR. High SpxA2 levels as a result of LiaFSR activation were directly correlated with increased CovR-regulated virulence gene transcription. Further, consistent with known virulence gene repression by phosphorylated CovR, elevated SpxA2 levels were inversely correlated with CovR phosphorylation. Despite increased transcription of several virulence factors, DliaF (high SpxA2) exhibited a paradoxical virulence phenotype in both in vivo mouse and ex vivo human blood models of disease. Likewise, despite decreased virulence factor transcription in DliaR (low SpxA2), increased virulence was observed in an in vivo mouse model of disease – a phenotype attributable, in part, to known SpxA2-associated speB transcription. Our findings provide evidence of a critical role of LiaFSR in sensing the host environment and suggest a potential mechanism for gene regulatory system crosstalk shared by many Gram-positive pathogens.
2021-08-05 | GSE181516 | GEO
Project description:Transcriptional profiling of Streptococcus pyogenes MGAS5005 cells comparing control untreated GAS cells with GAS cells exposed to 4uM heme for 1.5 h Two-condition experiment, untreated vs. heme-treated MGAS5005 cells. Biological replicates: 3 control, 3 Heme-treated, independantly grown and harvested. One replicate per array.
2014-09-16 | E-GEOD-61415 | biostudies-arrayexpress
Project description:The nasopharynx and the skin are the major oxygen-rich anatomical sites for colonization by the human pathogen Streptococcus pyogenes (group A Streptococcus, GAS). To establish infection, GAS must survive oxidative stress generated during aerobic metabolism and the release of reactive oxygen species (ROS) by host innate immune cells. Glutathione is the major host antioxidant molecule while GAS is glutathione-auxotrophic. Here we report the molecular characterization of the ABC transporter substrate binding protein GshT in the GAS glutathione salvage pathway. We demonstrate that glutathione uptake is critical for aerobic growth of GAS and that impaired import of glutathione induces oxidative stress that triggers enhanced production of the reducing equivalent NADPH. Our results highlight the interrelationship between glutathione assimilation, carbohydrate metabolism, virulence factor production and innate immune evasion. Together, these findings suggest an adaptive strategy employed by extracellular bacterial pathogens to exploit host glutathione stores for their own benefit.
2022-04-04 | GSE198061 | GEO