Journal Article10.1046/J.1365-2958.1997.2311591.X
A cloned pathogenicity island from enteropathogenic Escherichia coli confers the attaching and effacing phenotype on E. coli K‐12
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TL;DR: Cloned a 35.4 kb ‘pathogenicity island’ from the prototype AE bacterium, enteropathogenic Escherichia coli, containing all previously described AE genes, demonstrating that the defining feature of this class of pathogens can be acquired by an avirulent bacterium in a single genetic step.
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Abstract: Attaching and effacing (AE) bacteria are a diverse group of gastrointestinal pathogens, comprising members of four genera, that cause the intestinal epithelial microvilli to be replaced with raised clusters of filamentous actin that conform to the surface of attached bacteria. We have cloned a 35.4 kb ‘pathogenicity island’ from the prototype AE bacterium, enteropathogenic Escherichia coli, containing all previously described AE genes. Transfer of this pathogenicity island to avirulent E. coli converts the recipients into strains that secrete virulence proteins, induce host signal-transduction pathways, and cause AE lesions on cultured epithelial cells. These results demonstrate that this pathogenicity island contains all pathogen-specific genes necessary for inducing AE lesions, and that the defining feature of this class of pathogens can be acquired by an avirulent bacterium in a single genetic step.
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Citations
Characterization of translocation pores inserted into plasma membranes by type III‐secreted Esp proteins of enteropathogenic Escherichia coli
TL;DR: These results, together with the homologies of EspB and EspD to proposed functional domains of other pore‐forming proteins (Yop/Ipa), strongly support the idea that both proteins are directly involved in pore formation, which might represent the type III secretion system translocon.
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Transcriptional regulation of type III secretion genes in enteropathogenic Escherichia coli: Ler antagonizes H-NS-dependent repression.
TL;DR: The results suggest that Ler acts as an antirepressor protein that overcomes the H‐NS‐mediated silencing on the LEE2/LEE3 divergent promoter region, which is probably caused by the formation of a repressing H‐ NS–nucleoprotein complex.
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Locus of Enterocyte Effacement from Citrobacter rodentium: Sequence Analysis and Evidence for Horizontal Transfer among Attaching and Effacing Pathogens
TL;DR: The results indicate that the full DNA sequence of C.rodentium LEE has been acquired by C. rodentium and A/E E.coli strains independently during evolution.
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Versatile insertion plasmids for targeted genome manipulations in bacteria: isolation, deletion, and rescue of the pathogenicity island LEE of the Escherichia coli O157:H7 genome.
TL;DR: A system of versatile insertion plasmids was constructed that permits efficient delivery of the target sites of an ultra-rare-cutting endonuclease and the recombinase FLP into preselected sites of the bacterial genome.
Enteropathogenic and enterohemorrhagic Escherichia coli virulence gene regulation.
TL;DR: Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) cause significant morbidity and mortality worldwide while EHEC disease appears in primarily industrialized nations yet causes fewer disease outbreaks in developing countries.
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References
A genetic locus of enterocyte effacement conserved among diverse enterobacterial pathogens.
TL;DR: It is reported that in EPEC a 35-kbp locus containing several regions implicated in formation of these lesions is found, which hybridize to E. coli O157:H7 and other pathogens of three genera that cause similar lesions but do not hybridized to avirulent members of the same species.
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A genetic locus of enteropathogenic Escherichia coli necessary for the production of attaching and effacing lesions on tissue culture cells.
TL;DR: The ability of enteropathogenic Escherichia coli to form attaching and effacing intestinal lesions is a major characteristic of EPEC pathogenesis and a chromosomal gene (eae) that is necessary for this activity is identified using TnphoA mutagenesis.
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Attaching and effacing activities of rabbit and human enteropathogenic Escherichia coli in pig and rabbit intestines.
TL;DR: Three strains of enteropathogenic Escherichia coli (EPEC), originally isolated from humans and previously shown to cause diarrhea in human volunteers by unknown mechanisms, and one rabbit EPEC strain were shown to attach intimately to and efface microvilli and cytoplasm from intestinal epithelial cells in both the pig and rabbit intestine.
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Enteropathogenic Escherichia coli contains a putative type III secretion system necessary for the export of proteins involved in attaching and effacing lesion formation
Karen G. Jarvis,Jorge A. Girón,Ann E. Jerse,Timothy K. McDaniel,Michael S. Donnenberg,James B. Kaper +5 more
TL;DR: The identified EPEC chromosomal genes whose predicted protein sequences are similar to components of a recently described secretory pathway (type III) responsible for exporting proteins lacking a typical signal sequence suggest that the EPEC Sep proteins are component of a type III secretory apparatus necessary for the export of virulence determinants.
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Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins
TL;DR: Results indicate that attachment of H. pylori to gastric epithelial cells resembles that of enteropathogenic Escherichia coli, and cytoskeletal components actin, alpha-actinin, and talin are involved in the process.
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