{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,6]],"date-time":"2025-10-06T06:05:41Z","timestamp":1759730741456},"reference-count":44,"publisher":"Microbiology Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,4,1]]},"abstract":"<jats:p>Shiga toxin-producing <jats:italic>Escherichia coli<\/jats:italic> (STEC) causes a spectrum of human illnesses such as haemorrhagic colitis and haemolytic\u2013uraemic syndrome. Although the locus of enterocyte effacement (LEE) seems to confer enhanced virulence, LEE-negative STEC strains are also associated with severe human disease, suggesting that other unknown factors enhance the virulence potential of STEC strains. A novel hybrid pathogenicity island, termed PAI I<jats:sub>CL3<\/jats:sub>, has been previously characterized in the LEE-negative O113\u200a:\u200aH21 STEC strain CL3. Screening for the presence of PAI I<jats:sub>CL3<\/jats:sub> elements in 469 strains of <jats:italic>E. coli<\/jats:italic>, including attaching and effacing (A\/E) pathogens [enteropathogenic <jats:italic>E. coli<\/jats:italic> (EPEC) and enterohaemorrhagic <jats:italic>E. coli<\/jats:italic> (EHEC)], non-A\/E pathogens [LEE-negative STEC, extra-intestinal pathogenic <jats:italic>E. coli<\/jats:italic> (ExPEC), enterotoxigenic <jats:italic>E. coli<\/jats:italic> (ETEC) and enteroaggregative <jats:italic>E. coli<\/jats:italic> (EAEC)] and commensal <jats:italic>E. coli<\/jats:italic> isolates, showed that PAI I<jats:sub>CL3<\/jats:sub> is unique to LEE-negative STEC strains linked to disease, providing a new marker for these strains. We also showed that a PAI I<jats:sub>CL3<\/jats:sub>-equivalent gene cluster is present in the genome of <jats:italic>Citrobacter rodentium<\/jats:italic>, on a 53\u2005kb genomic island inserted into the <jats:italic>pheV<\/jats:italic> tRNA locus. While the <jats:italic>C. rodentium<\/jats:italic> PAI I<jats:sub>CL3<\/jats:sub> shows high similarities at the nucleotide level and in organization with the <jats:italic>E. coli<\/jats:italic> PAI I<jats:sub>CL3<\/jats:sub>, the genetic context of the integration differs completely. In addition, <jats:sc>blast<\/jats:sc> searches revealed that other <jats:italic>E. coli<\/jats:italic> pathotypes (O157\u200a:\u200aH7 EHEC, ExPEC, EPEC and EAEC) possess incomplete PAI I<jats:sub>CL3<\/jats:sub> elements that contain only the genes located at the extremities of the island. Six of the 16 sequenced <jats:italic>E. coli<\/jats:italic> genomes showed deleted PAI I<jats:sub>CL3<\/jats:sub> gene clusters which are carried on mobile genetic elements inserted into <jats:italic>pheV<\/jats:italic>, <jats:italic>selC<\/jats:italic> or <jats:italic>serW<\/jats:italic> tRNA loci, which is compatible with the idea that the PAI I<jats:sub>CL3<\/jats:sub> gene cluster entered <jats:italic>E. coli<\/jats:italic> and <jats:italic>C. rodentium<\/jats:italic> at multiple times through independent events. The phylogenetic distribution of the PAI I<jats:sub>CL3<\/jats:sub> variants suggests that a B1 genetic background is necessary for the maintenance of the full complement of PAI I<jats:sub>CL3<\/jats:sub> genes in <jats:italic>E. coli<\/jats:italic>.<\/jats:p>","DOI":"10.1099\/mic.0.026807-0","type":"journal-article","created":{"date-parts":[[2009,3,31]],"date-time":"2009-03-31T07:52:51Z","timestamp":1238485971000},"page":"1016-1027","source":"Crossref","is-referenced-by-count":12,"title":["Genomic analysis of the PAI ICL3 locus in pathogenic LEE-negative Shiga toxin-producing Escherichia coli and Citrobacter rodentium"],"prefix":"10.1099","volume":"155","author":[{"given":"Jean Pierre","family":"Girardeau","sequence":"first","affiliation":[{"name":"INRA, UR454 Unit\u00e9 de Microbiologie, F-63122 Saint-Gen\u00e8s Champanelle, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yolande","family":"Bertin","sequence":"additional","affiliation":[{"name":"INRA, UR454 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