Pseudomonas aeruginosa coexpresses two distinct lipopolysaccharide (LPS) molecules known asPseudomonas aeruginosa is an opportunistic pathogen responsible for many debilitating infections, with one of the most notable being chronic pulmonary infections in cystic fibrosis patients. The pathogenicity of this organism is attributed to the production of such diverse virulence factors as exotoxin A, phospholipase C, proteases, alginate, and lipopolysaccharide (LPS). LPS molecules also play an essential structural role in the outer membrane and consist of three distinct regions: a hydrophobic lipid A, which serves to anchor the LPS in the outer membrane, a core oligosaccharide, and the O antigen (O polysaccharide). P. aeruginosa has been shown to coexpress two distinct forms of LPS, known as A band and B band. A-band LPS is an antigenically conserved molecule with an O-polysaccharide region composed of short-chained polymers of D-rhamnose, arranged as trisaccharide repeat units of ␣132, ␣133, and ␣133 linkages (2). In comparison, B-band LPS is serospecific, with variations in the O-antigen structure differentiating P. aeruginosa into 20 distinct serotypes (36,46,47). During chronic pulmonary infections in cystic fibrosis patients, P. aeruginosa isolates become nontypeable due to the loss of B-band O antigen, while A-band LPS and alginate become the primary surface polysaccharides (22, 42). To determine the mechanisms involved in P. aeruginosa LPS biosynthesis and regulation, our laboratory has focused on identifying and characterizing genes involved in A-band and B-band synthesis and expression.