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Microbiology 143 (1997), 3461-3471; DOI  10.1099/00221287-143-11-3461
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Flagellar flhA, flhB and flhE genes, organized in an operon, cluster upstream from the inv locus in Yersinia enterocolitica

Alan Fauconnier1,4, Abdelmounaaïm Allaoui2,{dagger}, Andrés Campos3,{ddagger}, Ary Van Elsen1, Guy R. Cornelis2 and Alex Bollen1

1Applied Genetics, Université Libre de Bruxelles, Rue de I'Industrie 24, B-1400 Nivelles, Belgium
2Microbial Pathogenesis Unit, International Institute of Cellular and Molecular Pathology and Faculté de Médecine, Université Catholique de Louvain, Avenue Hippocrate 74, B-1200 Bruxelles, Belgium
3Departamento de Bioenergética, Institute de Fisiologia Celular, Universidad Nacional Autónoma de México, México 04510 DF, Mexico

4 Author for correspondence: Alan Fauconnier. Tel: + 32 67 889 425. Fax: +32 67 889 472. e-mail: afaucon@sga.ulb.ac.be

ABSTRACT

The inv gene of Yersinia enterocolitica codes for invasin, a member of the invasin/intimin-like protein family, which mediates the internalization of the bacterium into cultured epithelial cells. The putative inclusion of inv into a pathogenicity island was tested by investigating its flanking sequences. Indeed, the enteropathogenic Escherichia coli (EPEC) intimin, a member of the same family of proteins, is encoded by eaeA, a gene which belongs to a pathogenicity island. An ORF located upstream from inv was of particular interest since it appeared homologous both to the flagellar flhA gene and to sepA, an EPEC gene lying inside the same pathogenicity island as eaeA. A mutant in this ORF was non-motile and non-flagellated while its invasion phenotype remained unaffected. These data indicated that the ORF corresponded to the flhA gene of Y. enterocolitica. Subsequently, the flhB and flhE genes, located respectively upstream and downstream from flhA, were identified. The three flh genes appear to be transcribed from a single operon called flhB, according to the nomenclature used for Salmonella typhimurium. Intergenic sequence between flhE and inv includes a grey hole, with no recognizable function. Downstream from inv, we have detected the flagellar flgM operon as already reported. Finally, the incongruous localization of inv amidst the flagellar cluster is discussed; while transposition could explain this phenomenon, no trace of such an event was detected.


Keywords: Yersinia enterocolitica, invasin, LcrD/FlbF, flagellar genes, motility

{ddagger} Present address: Department of Microbiology and Immunology, College of Medicine, E-603 Medical Science Building, 835, South Wolcott Avenue, Chicago, IL 60612-7344, USA.

{dagger} Present address: Department of Microbiology, Medical School, University of Newcastle-upon-Tyne, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK.




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