migA, a quorum-responsive gene of Pseudomonas aeruginosa, is highly expressed in the cystic fibrosis lung environment and modifies low-molecular-masslipopolysaccharide

Pseudomonas aeruginosa is an opportunistic human pathogen which poses a maj or threat to patients with cystic fibrosis (CF). Excessive amounts of mucus present in the lungs of CF patients promotes the colonization of P. aerugi nosa, The migA gene, encoding a putative glycosyltransferase, has been show n to be highly inducible by respiratory mucus derived from CF patients. In this study, it is further demonstrated by population transcript analysis th at the migA gene is highly expressed in the CF lung environment. Deletion a nalysis of the migA promoter identified a las-box-like sequence commonly fo und in promoters that are responsive to quorum sensing regulation. Further analysis of migA expression in quorum-sensing-defective strains, as well as its expression in response to autoinducer molecules, demonstrated that mig A is regulated by the RhII/RhIR quorum sensing regulatory system. Functiona lly, as the MigA sequence homology data suggested, the migA gene indeed aff ects the structure of LPS in P, aeruginosa. Increased expression of the mig A gene results in a loss of core-plus-one LPS, while having no obvious effe ct on the long-chain O-antigen-bearing LPS. Although the exact biological r ole of the core-plus-one LPS is not clear, these experimental results sugge st that migA up-regulation in the CF lung environment is part of the adapti ve response which confers on P, aeruginosa a survival advantage.