Summary: The genes of and encode the filament-cap protein of the flagellar apparatus, which facilitates the polymerization of endogenous flagellin at the tips of the growing filaments. Previous sequence analysis of this operon in both organisms has revealed that the gene constitutes an operon together with two additional genes, and . Based on the gene-disruption experiment in , both the and genes have been postulated to be necessary for flagellation. In the present study, we constructed mutants in which either or on the chromosome was specifically disrupted. Both mutants were found to produce functional flagella, indicating that these genes are dispensable for motility development in . However, flagellar filaments produced by the mutant were much shorter than those produced by the wild-type strain. This indicates that the mutation affects the elongation step of filament assembly. The excretion efficiency of flagellin was examined in the -mutant background, where the exported flagellin molecules cannot assemble onto the hooks, resulting in their excretion into the culture media. We found that the amount of flagellin excreted was much reduced by the mutation. Based on these results, we conclude that FliS facilitates the export of flagellin through the flagellum-specific export pathway.


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