Flagellar flhA, flhB and flhE genes, organized in an operon, cluster upstream from the inv locus in Yersinia enterocolitica

Abstract

The inv gene of Yeminis enterocolitica codes for invasin, a member of the invasinhtimin-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 f/hA 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. lntergenic sequence between f/hE 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.

Requirement offlhAfor Swarming Differentiation, Flagellin Export, and Secretion of Virulence-Associated Proteins inBacillus thuringiensis

“…B. thuringiensis flhA is necessary for the export of flagellin but not for its synthesis. Enteric bacteria and B. subtilis carrying mutations in flhA exhibit a nonflagellated phenotype, and the mutation in flhA has been demonstrated to be the only factor responsible for the lack of flagellar assembly in the mutant strains (12,16,20,35). Indeed, flhA mutants are completely defective in the export of the anti-sigma factor FlgM, which downregulates the expression of flagellar class III genes, flagellin included (44).…”

A new pathway for the secretion of virulence factors by bacteria: The flagellar export apparatus functions as a protein-secretion system

“…Similarly, no YplA activity or export was detected when ptac-yplA was expressed in strains carrying mutations in class II genes such as flgE, flgF, flhA, or flhB (Table 2 and data not shown). These class II genes encode subunits of the flagellum basal body including the type III secretion machinery (4,21). For each of these secretion-defective strains, expression of ptac-yplA resulted in YplA production, but it was only detected in whole-cell fractions and appeared to be rapidly degraded.…”

The Yersinia enterocolitica Phospholipase Gene yplA Is Part of the Flagellar Regulon

“…The expression of class II flagellar genes encoding this apparatus is dependent on FlhDC but does not require FliA or expression of the class III genes. Interestingly, the class II flagellar genes flhBAE of Y. enterocolitica are not transcriptionally regulated by temperature (14). As FlhA and FlhB are thought to be part of the secretion apparatus (1, 30), a functional flagellar type III secretion apparatus may be produced at 37°C although the flagellum is not complete and the yersiniae are not motile.…”

“…The flagellar sigma factor ( F or FliA) directs transcription of class III genes, and fliA itself is temperature regulated (24). However, transcription of the class II flagellar genes flhBAE was unaffected by a shift to 37°C (14). By analogy to Escherichia coli and salmonellae, class II flagellar proteins form a transmembrane structure which serves as the flagellar type III secretion apparatus (1).…”