Molecular Characterization of Three Tandemly Located Flagellin Genes of Stenotrophomonas maltophilia

Abstract

Stenotrophomonas maltophilia is a motile, opportunistic pathogen. The flagellum, which is involved in swimming, swarming, adhesion, and biofilm formation, is considered a virulence factor for motile pathogens. Three flagellin genes, fliC1, fliC2, and fliC3, were identified from the sequenced S. maltophilia genome. FliC1, fliC2, and fliC3 formed an operon, and their encoding proteins shared 67–82% identity. Members of the fliC1C2C3 operon were deleted individually or in combination to generate single mutants, double mutants, and a triple mutant. The contributions of the three flagellins to swimming, swarming, flagellum morphology, adhesion, and biofilm formation were assessed. The single mutants generally had a compromise in swimming and no significant defects in swarming, adhesion on biotic surfaces, and biofilm formation on abiotic surfaces. The double mutants displayed obvious defects in swimming and adhesion on abiotic and biotic surfaces. The flagellin-null mutant lost swimming ability and was compromised in adhesion and biofilm formation. All tested mutants demonstrated substantial but different flagellar morphologies, supporting that flagellin composition affects filament morphology. Bacterial swimming motility was significantly compromised under an oxidative stress condition, irrespective of flagellin composition. Collectively, the utilization of these three flagellins for filament assembly equips S. maltophilia with flagella adapted to provide better ability in swimming, adhesion, and biofilm formation for its pathogenesis.

Roles of Hcp2, a Hallmark of T6SS2 in Motility, Adhesive Capacity, and Pathogenicity of Vibrio alginolyticus

“…FlrA is another important master regulon that initiates flagellar gene expression in an RpoN-dependent manner, which is required for proper flagellation and includes the polar flagellar number and morphology related to bacterial motility [48]. Additionally, another study found that flagellin mutants or flrA-, flrB-, or flrC-silenced strains affect filament morphology and the swimming, adhesion, and biofilm formation ability for its pathogenesis in Stenotrophomonas maltophilia and Vibrio alginolyticus [49,50]. Hence, we investigated whether the transcriptional levels of these flagellar regulons were affected by hcp2.…”