title: migA, a quorum-responsive gene of Pseudomonas aeruginosa, is highly expressed in the cystic fibrosis lung environment and modifies low-molecular-mass lipopolysaccharide.
abstract: Pseudomonas aeruginosa is an opportunistic human pathogen which poses a major threat to patients with cystic fibrosis (CF). Excessive amounts of mucus present in the lungs of CF patients promotes the colonization of P. aeruginosa. The migA gene, encoding a putative glycosyltransferase, has been shown to be highly inducible by respiratory mucus derived from CF patients. In this study, it is further demonstrated by population transcript analysis that the migA gene is highly expressed in the CF lung environment. Deletion analysis of the migA promoter identified a las-box-like sequence commonly found 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 migA is regulated by the RhlI/RhlR quorum sensing regulatory system. Functionally, as the MigA sequence homology data suggested, the migA gene indeed affects the structure of LPS in P. aeruginosa. Increased expression of the migA gene results in a loss of core-plus-one LPS, while having no obvious effect on the long-chain O-antigen-bearing LPS. Although the exact biological role of the core-plus-one LPS is not clear, these experimental results suggest that migA up-regulation in the CF lung environment is part of the adaptive response which confers on P. aeruginosa a survival advantage.
authors.affiliation: Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA1.
authors.forename: Hongjiang
authors.initials: H
authors.lastname: Yang
authors.affiliation: Department of Microbiology, University of Guelph, Guelph, Ontario, Canada2.
authors.forename: Mauricia
authors.initials: M
authors.lastname: Matewish
authors.affiliation: Department of Biological Sciences, University of Calgary, Calgary, Canada3.
authors.forename: Isabelle
authors.initials: I
authors.lastname: Loubens
authors.affiliation: Department of Biological Sciences, University of Calgary, Calgary, Canada3.
authors.forename: Douglas G
authors.initials: DG
authors.lastname: Storey
authors.affiliation: Department of Microbiology, University of Guelph, Guelph, Ontario, Canada2.
authors.forename: Joseph S
authors.initials: JS
authors.lastname: Lam
authors.affiliation: Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA1.
authors.forename: Shouguang
authors.initials: S
authors.lastname: Jin
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism*; D001483:Base Sequence; D003550:Cystic Fibrosis / Q000382:microbiology*; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D016695:Glycosyltransferases / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D008070:Lipopolysaccharides / Q000737:chemistry / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000382:microbiology*; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D011552:Pseudomonas Infections / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000201:enzymology* / Q000235:genetics; D015398:Signal Transduction; D013183:Sputum / Q000378:metabolism / Q000382:microbiology
chemical_list: D001426:Bacterial Proteins; D008070:Lipopolysaccharides; C417484:MigA protein, Pseudomonas aeruginosa; D016695:Glycosyltransferases