Pseudomonas aeruginosa colonizes the mucus of patients with chronic lung diseases by a specific mechanism involving an adhesin-receptor system. Several adhesins have been implicated in the adhesion of P. aeruginosa to cells, but the identity of the principal adhesin(s) involved in adhesion to mucin is unknown. Mutagenesis studies have indicated that P. aeruginosa adhesion is under the control of the rpoN gene, which also regulates pilin synthesis, flagellum formation, and other functions. Mutagenesis of certain flagellar genes that are not controlled by RpoN, e.g., flif, also indicates a close relationship between adhesion and flagellar genes and not necessarily an independent effect of rpoN on adhesion. Mutants of certain early flagellar genes lead to the loss of both adhesion and motility, whereas mutants of certain late genes, e.g., fliC, the gene for flagellin, lose motility but retain adhesion. Recent studies indicate that both motility and adhesion are regulated by a two-component regulatory system called fleS-R, which in turn is controlled by another regulator in a cascade that involves rpoN. A fleR mutant possessing pili adheres poorly to mucins, definitively showing that pili do not play a major role in adhesion to mucin. It is unclear whether the adhesin is a flagellar protein or another protein that uses the flagellar export apparatus for localization or both. Finding the gene under control of rpoN may provide answers to these questions.