The effect of pdhR deletion on virulence in E. coli O157:H7
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB74273 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12796663.fastq.gz | Fastqsanger.gz | |||
| ERR12796664.fastq.gz | Fastqsanger.gz | |||
| ERR12796665.fastq.gz | Fastqsanger.gz | |||
| ERR12796666.fastq.gz | Fastqsanger.gz | |||
| ERR12796667.fastq.gz | Fastqsanger.gz |
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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:Integrating laterally acquired virulence genes into the backbone regulatory network is important for the pathogenesis of Escherichia coli O157:H7, which has captured many virulence genes through horizontal transfer during evolution. GadE is an essential transcriptional activator of glutamate decarboxylase (GAD) system, the most efficient acid resistance mechanism in E. coli. The full contribution of GadE to the acid resistance and virulence of pathogenic E. coli O157:H7 remains largely unknown. We inactivated gadE in E. coli O157:H7 Sakai and compared global transcription profiles with that of wild type in exponential and stationary phases of growth using microarrays containing 6088 ORFs from three E. coli genomes. gadE inactivation significantly altered the expression of 60 genes independent of growth phase and 122 genes in a growth phase-dependent manner. Inactivation of gadE markedly down-regulated the expression of gadA, gadB, gadC and many acid fitness island genes in a growth phase-dependent manner. Nineteen genes encoded on the locus of enterocyte effacement (LEE), including ler, showed a significant increase in expression upon gadE inactivation. Altogether, our data indicate that GadE is critical for acid resistance of E. coli O157:H7 and plays an important role in virulence by down-regulating expression of LEE.
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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. 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.
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Project description:RpoS is a conserved stress regulator that plays a critical role in survival under stress conditions in Escherichia coli and other γ-proteobacteria. RpoS is also involved in virulence of many pathogens including Salmonella and Vibrio species. Though well characterized in non-pathogenic E. coli K12 strains, the effect of RpoS on transcriptome expression has not been examined in pathogenic isolates. E. coli O157:H7 is a serious human enteropathogen, possessing a genome 20% larger than that of E. coli K12, and many of the additional genes are required for virulence. The genomic difference may result in substantial changes in RpoS-regulated gene expression. To test this, we compared the transcriptional profile of wild type and rpoS mutants of the E. coli O157:H7 EDL933 type strain. The rpoS mutation had a pronounced effect on gene expression in stationary phase, and more than 1,000 genes were differentially expressed (two-fold, p<0.05). By contrast, we found 11 genes expressed differently in exponential phase. Western blot analysis revealed that, as expected, RpoS level was low in exponential phase and substantially increased in stationary phase. The defect in rpoS resulted in impaired expression of genes responsible for stress response (e.g., gadA, katE and osmY), arginine degradation (astCADBE), putrescine degradation (puuABCD), fatty acid oxidation (fadBA and fadE), and virulence (ler, espI and cesF). For EDL933-specific genes on O-islands, we found 50 genes expressed higher in wild type EDL933 and 49 genes expressed higher in the rpoS mutants. The protein levels of Tir and EspA, two LEE-encoded virulence factors, were elevated in the rpoS mutants under LEE induction conditions. Our results show that RpoS has a profound effect on global gene expression in the pathogenic strain O157:H7 EDL933, and the identified RpoS regulon, including many EDL933-specific genes, differs substantially from that of laboratory K12 strains. In this study, we characterized the RpoS regulon of E. coli O157:H7 strain EDL933 using microarray analysis.
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