Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA111139 | ENA |
REPOSITORIES: ENA
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Project description:Escherichia coli O157:H7 is a food-borne pathogen that causes bloody diarrhea and hemolytic uremic syndrome. Hfq is an sRNA chaperone protein that is involved in post-transcriptional regulation of virulence genes in pathogenic bacteria. In EHEC strain EDL933, Hfq acts a negative regulator of the locus of enterocyte effacement (LEE) that encodes most of the proteins involved in type three secretion and attaching and effacing lesions. We deleted hfq in E. coli O157:H7 strain 86-24 and compared global transcription profiles of the hfq mutant to the wild type strain in exponential growth phase. Deletion of hfq affected transcription of genes common to nonpathogenic and pathogenic strains of E. coli as well as pathogen-specific genes. Downregulated genes in the hfq mutant included ler as well as genes encoded in LEE2-5 that encode for type three secretion and AE lesion formation. Decreased expression of the LEE genes in the hfq mutant occurred at mid-, late, and stationary growth phases in both LB and DMEM media as detected by qRT-PCR. We also confirmed decreased regulation of the LEE genes by examining secreted proteins and AE lesion formation by the hfq mutant and WT strains. Deletion of hfq also caused decreased expression of the two-component system qseBC involved in inter-kingdom signaling and virulence gene regulation in EHEC as well as an increase in stx2AB expression that encodes for the deadly Shiga toxin. Altogether, these data indicate that Hfq plays a different regulatory role in EHEC 86-24 from what has been reported for EHEC strain EDL933 and that the role of Hfq in EHEC virulence regulation extends beyond the LEE.
2012-01-06 | GSE30893 | GEO
Project description:QseA regulation of virulence factors in EHEC
| PRJNA119441 | ENA
Project description:Escherichia coli O157:H7 is a food-borne pathogen that causes bloody diarrhea and hemolytic uremic syndrome. Hfq is an sRNA chaperone protein that is involved in post-transcriptional regulation of virulence genes in pathogenic bacteria. In EHEC strain EDL933, Hfq acts a negative regulator of the locus of enterocyte effacement (LEE) that encodes most of the proteins involved in type three secretion and attaching and effacing lesions. We deleted hfq in E. coli O157:H7 strain 86-24 and compared global transcription profiles of the hfq mutant to the wild type strain in exponential growth phase. Deletion of hfq affected transcription of genes common to nonpathogenic and pathogenic strains of E. coli as well as pathogen-specific genes. Downregulated genes in the hfq mutant included ler as well as genes encoded in LEE2-5 that encode for type three secretion and AE lesion formation. Decreased expression of the LEE genes in the hfq mutant occurred at mid-, late, and stationary growth phases in both LB and DMEM media as detected by qRT-PCR. We also confirmed decreased regulation of the LEE genes by examining secreted proteins and AE lesion formation by the hfq mutant and WT strains. Deletion of hfq also caused decreased expression of the two-component system qseBC involved in inter-kingdom signaling and virulence gene regulation in EHEC as well as an increase in stx2AB expression that encodes for the deadly Shiga toxin. Altogether, these data indicate that Hfq plays a different regulatory role in EHEC 86-24 from what has been reported for EHEC strain EDL933 and that the role of Hfq in EHEC virulence regulation extends beyond the LEE. Comparison of transcriptional regulation of the WT 86-24 isolate and the hfq mutant for the identification of regulated targets that were followed up by functional analysis.
2012-01-06 | E-GEOD-30893 | biostudies-arrayexpress
Project description:Enteric pathogens with low infectious doses rely on the ability to orchestrate expression of virulence and metabolism-associated genes in response to environmental cues for successful infection. Accordingly, the human pathogen enterohemorrhagic Escherichia coli (EHEC) employs a complex multifaceted regulatory network to link expression of type III secretion system (T3SS) factors to nutrient availability. While phosphorylation of histidine and aspartate on two-component system response regulators is recognized as an integral part of signaling, the involvement of phosphotyrosine-mediated control is minimally explored in Gram-negative pathogens. Our recent phosphotyrosine profiling study of E. coli revealed 342 proteins, indicating that phosphotyrosine modifications in bacteria are more prevalent than previously anticipated. Here, we demonstrate that tyrosine phosphorylation of a metabolite-responsive LacI/GalR family regulator, Cra, negatively affects T3SS expression in glycolytic conditions typical for the colon lumen environment where production of the T3SS is unnecessary. Our data suggest that Cra phosphorylation affects T3SS expression by modulating expression of ler, encoding the major activator of EHEC virulence gene expression. Phosphorylation of the Cra Y47 residue diminishes DNA-binding, thereby altering expression of metabolism and virulence-associated genes including those of the LEE pathogenicity island encoding the T3SS. Hence, phosphotyrosine-mediated regulation provides a mechanism to regulate Cra activity. Our data further suggest that tyrosine phosphorylation influences DNA binding by PurR and LacI, thereby phosphotyrosine-mediated control could provide a means to regulate DNA-binding of LacI/GalR family regulators in general. Our study provides an initial effort to unravel the role of phosphotyrosine-mediated global signaling in controlling the EHEC virulence potential
2018-02-02 | GSE103764 | GEO
Project description:Previous studies have shown serotonin and indole downregulate expression of virulence genes in EHEC, here we demonstrate the combinatorial effect of serotonin and indole on EHEC transcriptome
2025-08-12 | GSE296573 | GEO
Project description:In 2011, in Germany, Escherichia coli O104:H4 caused the enterohemorrhagic E. coli (EHEC) outbreak with the highest incidence rate of hemolytic uremic syndrome. This pathogen carries an exceptionally potent combination of EHEC- and enteroaggregative E. coli (EAEC)-specific virulence factors. Here, we identified an E. coli O104:H4 isolate that carried a single nucleotide polymorphism (SNP) in the start codon (ATG>ATA) of rpoS, encoding the alternative sigma factor S. The rpoS ATG>ATA SNP was associated with enhanced EAEC-specific virulence gene expression. Deletion of rpoS in E. coli O104:H4 Dstx2 and typical EAEC resulted in a similar effect. Both rpoS ATG>ATA and DrpoS strains exhibited stronger virulence-related phenotypes in comparison to wild type. Using promoter-reporter gene fusions, we demonstrated that wild-type RpoS repressed aggR, encoding the main regulator of EAEC virulence. In summary, our work demonstrates that RpoS acts as a global repressor of E. coli O104:H4 virulence, primarily through an AggR-dependent mechanism.
2024-04-04 | GSE243699 | GEO
Project description:Global regulation of the effects of deletion of phage cro gene in EHEC
2016-09-29 | GSE86271 | GEO
Project description:Enterococcus faecalis downregulates virulence genes of EHEC
| PRJNA339823 | ENA