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Conversion to a mucoid, exopolysaccharide alginate-overproducing phenotype in Pseudomonas aeruginosa is associated with chronic respiratory infections in cystic fibrosis. Mucoidy is caused by muc mutations that derepress the alternative sigma factor AlgU, which in turn activates alginate biosynthetic and ancillary regulatory genes. Here we report the(More)
The alternative sigma factor AlgU (Pseudomonas aeruginosa sigma E) is required for full resistance of P. aeruginosa to oxidative stress and extreme temperatures. AlgU also controls conversion of P. aeruginosa to the mucoid, alginate-overproducing phenotype associated with lethal infections in cystic fibrosis patients. Mutations that cause conversion to(More)
A distinguishing feature of Pseudomonas aeruginosa isolates from cystic fibrosis (CF) patients is their mucoid, exopolysaccharide alginate-overproducing phenotype. One mechanism of conversion to mucoidy is based on mutations in the algU mucABCD cluster, encoding the stress sigma factor AlgU and its regulators. However, conversion to mucoidy in laboratory(More)
The conversion to mucoid, exopolysaccharide alginate-overproducing phenotype in Pseudomonas aeruginosa during chronic respiratory infections in cystic fibrosis patients occurs via mutations that activate the alternative sigma factor AlgU (sigmaE). In this study, we demonstrate that conversion to mucoidy can be caused via a second, algU-independent pathway,(More)
A discerning feature of Pseudomonas aeruginosa strains causing chronic endobronchial infections in cystic fibrosis is their conversion into the mucoid, exopolysaccharide alginate-overproducing phenotype. This morphologically prominent change is caused by mutations which upregulate AlgU (sigma(E)), a novel extreme-stress sigma factor with functional(More)
Pseudomonas aeruginosa mutants that overproduce the exopolysaccharide alginate and assume mucoid phenotype are associated with the establishment of chronic respiratory disease in cystic fibrosis. The initially invading strains are nonmucoid and frequently convert into the mucoid form. Mucoidy is regulated at the transcriptional level, mainly at the promoter(More)
The study of the biosynthesis of alginate, the exopolysaccharide produced by Azotobacter vinelandii and Pseudomonas aeruginosa, has biotechnological and medical significance. We report here the identification of the A. vinelandii genes coding for the putative sigma factor AlgU and its negative regulators MucA and MucB through the suppression of the highly(More)
The CFTR gene encodes a transmembrane conductance regulator, which is dysfunctional in patients with cystic fibrosis (CF). The mechanism by which defective CFTR (CF transmembrane conductance regulator) leads to undersialylation of plasma membrane glycoconjugates, which in turn promote lung pathology and colonization with Pseudomonas aeruginosa causing(More)
Overproduction of the exopolysaccharide alginate causes mucoid colony morphology in Pseudomonas aeruginosa and is considered a major virulence determinant expressed by this organism during chronic respiratory infections in cystic fibrosis. One of the principal regulatory elements governing conversion to mucoidy in P. aeruginosa is AlgU, an alternative sigma(More)