Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA149913 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Global regulation of the effects of deletion of phage cro gene in EHEC
2016-09-29 | GSE86271 | GEO
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:Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. Here, we used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess the host colonic epithelial and lamina propria cell transcriptional responses to EHEC infection. Furthermore, comparisons of colonic pathology and intestinal transcriptomic profiles in animals infected with EHEC strains containing or lacking Shiga toxins (∆∆stx) were carried out to investigate how these potent toxins shape the host response to the pathogen. We found that Stx is required for severe, multi-focal hemorrhage and extensive apoptosis in the colon. RNA-sequencing revealed that EHEC infection elicits a robust innate immune response in the colonic epithelium that is dramatically shaped by Stx. Over 1400 genes were differentially expressed in animals infected with WT versus ∆∆stx EHEC strains. Several pathways linked to innate immune responses were dependent on Stx. Upregulated genes in the presence of toxin included cytokines IL23a and CXCL8, as well as F3, the gene encoding the coagulation initiator Tissue Factor. RNA FISH revealed that these elevated transcripts were found almost exclusively in epithelial cells, suggesting that Stx remodels the transcriptional profile of the epithelium. Collectively, these findings reveal that Stx potently modulates the innate immune response to EHEC in the intestine, and suggest that Stx drives the response to infection towards type 3 immunity.
2021-01-14 | GSE156056 | GEO
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: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: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:Contamination with enterohemorrhagic Escherichia coli O157:H7 (EHEC) is a worldwide problem but there is no effective therapy available for EHEC infection. Biofilm formation is closely related with EHEC infection and is one of the mechanisms of antimicrobial resistance. Antibiofilm screening of 560 plant secondary metabolites against EHEC shows that ginkgolic acids C15:1 and C17:1 at 5 μg/ml and Ginko biloba extract at 100 μg/ml significantly inhibited EHEC biofilm formation on the surface of polystyrene, nylon membrane, and glass. Importantly, the working concentration of ginkgolic acids and G. biloba extract did not affect bacterial growth and has been known to be non-toxic to human. Transcriptional analyses showed that ginkgolic acid C15:1 repressed curli genes and prophage genes in EHEC, which were corroborated by reduced fimbriae production and biofilm reduction in EHEC. Interestingly, ginkgolic acids and G. biloba extract did not inhibit the biofilm formation of commensal E. coli K-12 strain. The current study suggests that plant secondary metabolites are important resource of biofilm inhibitors, as well as other bioactive compounds.
2015-07-29 | GSE49367 | GEO
Project description:Transcriptional analysis of the effects of the deletion of the sRNAs glmY and glmZ in EHEC
2015-02-01 | GSE63336 | GEO
Project description:Analysis of effect of deletion of the two transcriptional factors KdpE and Cra on gene expression of EHEC 8624
2013-07-03 | GSE43659 | GEO