Fig. 12

A lack of Prc protease activity was responsible for the defective motility and decreased FliC expression in the prc mutant. (a) Motility diameters of the strains expressing wild-type Prc, Prc S430A, and Prc K455A. The results were derived from three independent experiments and are shown as the means ± standard deviations. (b) The protein levels of FliC, Prc, and OmpA in the bacteria expressing wild-type Prc, Prc S430A, and Prc K455A. The protein levels were determined by western blot analysis with a rabbit anti-FliC antiserum, rabbit anti-Prc antiserum and mouse anti-OmpA antiserum, respectively. The OmpA level served as a loading control. ΔfliC/pCL1920 served as a nonmobile and non-FliC expression control. pCL1920, the plasmid pCL1920, which served as an empty vector control. pPrc, the plasmid pCL1920 harboring prc; pPrc-S430A, the plasmid pCL1920 harboring a mutated prc expressing Prc S430A; pPrc-K455A, the plasmid pCL1920 harboring a mutated prc expressing Prc K455A