Analysis of the Pseudomonas aeruginosa Regulon Controlled by the Sensor Kinase KinB and Sigma Factor RpoN

摘要: Alginate overproduction by Pseudomonas aeruginosa, also known as mucoidy, is associated with chronic endobronchial infections in cystic fibrosis. biosynthesis initiated the extracytoplasmic function sigma factor (σ22; AlgU/AlgT). In wild-type (wt) nonmucoid strains, such PAO1, AlgU sequestered to cytoplasmic membrane anti-sigma MucA that inhibits alginate production. One mechanism underlying conversion mucoidy mutation of mucA. However, mucoid can occur wt mucA strains via degradation activated intramembrane proteases AlgW and/or MucP. Previously, we reported deletion sensor kinase KinB PAO1 induces an AlgW-dependent proteolysis MucA, resulting overproduction. This type induction requires alternate RpoN (σ54). To determine RpoN-dependent regulon, microarray and proteomic analyses were performed on a kinB mutant isogenic rpoN double mutant. controlled expression approximately 20% genome. addition biosynthetic regulatory genes, control large number genes including those involved carbohydrate metabolism, quorum sensing, iron regulation, rhamnolipid production, motility. acute pneumonia murine infection model, BALB/c mice exhibited increased survival when challenged relative challenge. Together, these data strongly suggest regulates virulence factors important for development mucoidy.