Escherichia coli E22
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ABSTRACT:
PROVIDER: PRJNA175771 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the regulatory targets of the RegR virulence regulon of rabbit specific enteropathogenic Escherichia coli strain E22
2012-12-25 | GSE41093 | GEO
Project description:To investigate the regulatory targets of the RegR virulence regulon of rabbit specific enteropathogenic Escherichia coli strain E22 Single factor (genotype) with dye swaps.
2012-12-25 | E-GEOD-41093 | biostudies-arrayexpress
Project description:Despite the characterization of many aetiologic genetic changes. The specific causative factors in the development of sporadic colorectal cancer remain unclear. This study was performed to detect the possible role of Enteropathogenic Escherichia coli (EPEC) in developing colorectal carcinoma.
| 2184564 | ecrin-mdr-crc
Project description:Many reports show an association between the Pst system, the Pho regulon related genes and bacterial virulence. Our previous results showed that a functional Pst system is required for full virulence, resistance to serum, polymyxin B and acid shock. However, the interplay between the Pst system and virulence has an unknown molecular basis. To understand global APEC virulent strain responses to Pho regulon activation, we conducted transcriptome profiling experiments comparing the APEC chi7122 strain and its isogenic Pst mutant grown in rich phosphate medium using the Affymetrix GeneChip® E. coli Genome 2.0 Array. The Affymetrix GeneChip® E. coli Genome 2.0 Array contains the genome of the E. coli MG1655 and three pathogenic E. coli strain (EDL933, Sakai and CFT073) representing 20,366 genes. While comparing genes expression between Pst mutant and the wild type chi7122 strain, 471 genes are either up- (254) or down-regulated (217) of at least 1.5-fold, with a p-value inferior or equal to 0.05 and a false discovery rate of 2.71%. Keywords: Escherichia coli, phosphate starvation response, Pho regulon, Pst system, Affymetrix, transcriptional analysis
2008-09-15 | GSE9178 | GEO
Project description:Atypical enteropathogenic Escherichia coli
| PRJNA15578 | ENA
Project description:Background: Members of E. coli serogroup O45 are porcine enteropathogenic E. coli (PEPEC) strains which cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most of O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors for A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC virulence. Methodology: Nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments. Results: Based on their virulence genes profiles, the 10 strains were characterized as atypical EPEC. The differences in their genomes pointed to two distinct evolutionary groups of O45 PEPEC, Group I and Group II, and to the contribution these genetic differences have on virulence in pigs. Group I contained the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of five other O45 PEPEC strains which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found in the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253).
2009-07-11 | GSE17036 | GEO
Project description:Background: Members of E. coli serogroup O45 are porcine enteropathogenic E. coli (PEPEC) strains which cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most of O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors for A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC virulence. Methodology: Nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments. Results: Based on their virulence genes profiles, the 10 strains were characterized as atypical EPEC. The differences in their genomes pointed to two distinct evolutionary groups of O45 PEPEC, Group I and Group II, and to the contribution these genetic differences have on virulence in pigs. Group I contained the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of five other O45 PEPEC strains which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found in the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253). 10 samples, with two microarrays per sample. Each microarray includes duplicates of every spot.
2010-05-16 | E-GEOD-17036 | biostudies-arrayexpress
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.
2009-08-03 | GSE17420 | 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