The fliD genes of Salmonella typhimurium and Escherichia coil encode t
he 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 fliD gene constitutes an operon together with t
wo additional genes, fliS and fliT. Based on the gene-disruption exper
iment in E. coli, both the fliS and fliT genes have been postulated to
be necessary for flagellation, In the present study, we constructed S
. typhimurium mutants in which either fliS or fliT on the chromosome w
as specifically disrupted. Both mutants were found to produce function
al flagella, indicating that these genes are dispensable for motility
development in S. typhimurium. However, flagellar filaments produced b
y the fliS mutant were much shorter than those produced by the wild-ty
pe strain. This indicates that the fliS mutation affects the elongatio
n step of filament assembly. The excretion efficiency of flagellin was
examined in the fliD-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 excrete
d was much reduced by the fliS mutation. Based on these results, we co
nclude that FliS facilitates the export of flagellin through the flage
llum-specific export pathway.