My primary goal was to examine the motility of mutants defective in the incorporation of L-rhamnose into the core oligosaccharide of lipopolysaccharide in 'P. aeruginosa' PAO1. A knockout mutant of 'rmlC' was constructed. Mutation in 'rmlC, migA, ' and 'wapR' resulted in reduced motility on soft-agar plates, altered attachment to surfaces, and increased hydrophobicity compared to the wild type. However, flagellar assembly and function appeared to be unaffected in these mutants. These results suggested that changes in cell-surface physicochemistry, caused by core oligosaccharide truncation, alter the attachment of the organism to surfaces, which in turn affects the movement of the organism. My secondary goal was to analyze flagellin from mutants deficient in L-rhamnose or D-rhamnose. This analysis indicated that L-rhamnose is incorporated into the flagellin glycan of 'P. aeruginosa' PAO1. These results demonstrated that biosynthetic precursors are shared between lipopolysaccharide and the flagellin glycan.