Streptococcus pyogenes strain:emm1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1003449 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26049000_1.fastq.gz | Fastqsanger.gz | |||
| SRR26049000_2.fastq.gz | Fastqsanger.gz | |||
| SRR26049100_1.fastq.gz | Fastqsanger.gz | |||
| SRR26049100_2.fastq.gz | Fastqsanger.gz | |||
| SRR26049001_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Streptococcus pyogenes emm1 causing invasive disease in Belgium (2020-2023)
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Project description:The human pathogen Streptococcus pyogenes, or group A streptococcus, is responsible for mild infections to life-threatening diseases. We previously have performed the transcription start site profiling of a Streptococcus pyogenes emm1 strain, strain S119, an invasive strain isolated from a blood culture. Here, we perform strand-specific RNA-seq experiments to complete this characterization and analyze the global coverage and the differential expression in growth medium complemented or not with 15 mM MgCl2. In addition we compare these results to those obtained with a related strain, strain S126, corresponding to a colonization sample, that differs from S119 by only one mutation in the two-component regulator of virulence CovRS.
2018-11-30 | E-MTAB-7101 | biostudies-arrayexpress
Project description:The human pathogen Streptococcus pyogenes, or group A streptococcus, is responsible for mild infections to life-threatening diseases. To determine the primary transcriptome of the emm1 strain S119, we have performed a differential RNA-Seq experiment based on selective Tobacco Acid Pyrophosphatase (TAP) treatment and 5' adapter ligation to differentiate primary transcripts (5' tri-phosphate) and processed RNAs (5' mono-phosphate). The libraries were performed on a mixture of RNAs prepared from bacteria cultured to late exponential phase in a rich growth culture medium supplemented or not with 15 mM of MgCl2
2018-11-30 | E-MTAB-7099 | biostudies-arrayexpress
Project description:Transcription start site profiling of a Streptococcus pyogenes emm1 strain
| PRJEB28014 | ENA
Project description:IGAS 2022-2023 upsurge - London non-invasive emm1 collection
| PRJEB71329 | ENA
Project description:Streptococcus pyogenes is a major causative agent of tonsillitis or pharyngitis in children, which can lead to more invasive infections and noninfectious sequellae. S. pyogenes can persist in tonsils, while one-third of children treated with antibiotics continue to shed streptococci and have recurrent infections. Mouse nasal-associated lymphoid tissue (NALT) is functionally analogous to human oropharangeal lymphoid tissues. The innate immune responses of naïve cells from a mucosal site to S. pyogenes is not well described; therefore, we infected C57BL/6 mice intranasally with 108 CFU S. pyogenes. Transcriptional responses by NALT after S. pyogenes infection were analyzed by Affymetrix microarray and quantitative RT-PCR. Wild-type S. pyogenes induces transcription of both type I and IFN-gamma-responsive genes, pro-inflammatory genes, and acute phase response plasma proteins within 24h after infection. Invasion of NALT and the induction of the interferon response were not dependent on expression of anti-phagocytic M1 protein. However, infection with an attenuated, less invasive mutant indicated that a robust innate response by NALT is significantly influenced by intra-NALT bacterial load. Granulocytic populations of NALT, cervical lymph nodes and spleen were discriminated by characteristic surface and intracellular markers. Intranasal infection induces systemic release of neutrophils and a substantial influx of neutrophils into NALT at 24h, which decline by 48h after infection. Macrophages do not significantly increase in S. pyogenes-infected NALT. Intranasal infection of IFN-gamma -/- (GKO) C57BL/6 mice did not lead to systemic dissemination of wild type S. pyogenes, despite reduced expression of IFN-gamma-responsive mRNAs in NALT. Infected GKO mice had an unregulated influx of neutrophils into NALT compared to immunocompetant mice and mice treated with an anti-IFN-gamma antibody more rapidly cleared S. pyogenes from NALT. Thus, IFN-gamma-induced responses have a suppressive influence on early clearance of this pathogen from NALT. Experiment Overall Design: C57BL/6 mice (6-10 weeks old), 4 per group, were infected intranasally with log-phase Streptococcus pyogenes, 2 to 4 x 10^8 CFU per 15 µl of pyrogen-free PBS. Sham-infected mice were administered 15 µl of the same PBS. Mice were infected with wild type strain 90-226 (Cue 1998), a 90-226 strain containing an in-frame deletion of M1 protein (90-226 delta emm1) (Zimmerlein 2005) or an attenuated 90-226 which lacks both M1 and SCPA proteins (90-226att). NALT was collected from mice at 24h after infection and stored in RNAlater until RNA could be purified).
2009-07-11 | E-GEOD-11494 | biostudies-arrayexpress
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
Project description:Whole genone expression profile comparing wild-type NZ131 to serR deletion mutant, grown in C-medium Mutants and interpretation are described further in the manuscript to be submitted: LaSarre and Federle, 2010. Title: Regulation and Consequence of Serine Catabolism in Streptococcus pyogenes. A two chip study using total RNA recovered from three separate wild-type cultures of Streptococcus pyogenes NZ131 and three separate mutant cultures of Streptococcus pyogenes NZ131 seR-, pooled following RNA extraction
2010-11-15 | E-GEOD-24860 | biostudies-arrayexpress
Project description:Streptococcus pyogenes (Group A Streptococcus: GAS) is a major human pathogen that causes streptococcal pharyngitis, skin and soft-tissue infections, and life-threatening conditions such as streptococcal toxic shock syndrome (STSS). A large number of virulence-related genes are encoded on GAS genomes, which are involved in host-pathogen interaction, colonization, immune invasion, and long-term survival within hosts, causing the diverse symptoms. Here, we investigated the interaction between GAS-derived extracellular vesicles and host cells in order to reveal pathogenicity mechanisms induced by GAS infection.
2021-05-17 | PXD026040 | JPOST Repository
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