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Background  Alginate overproduction in  P. aeruginosa , also referred to as mucoidy, is a poor prognostic marker for patients with cystic fibrosis (CF). We previously reported the construction of a unique mucoid strain which overexpresses a small envelope protein MucE leading to activation of the protease AlgW. AlgW then degrades the anti-sigma factor MucA thus releasing the alternative sigma factor AlgU/T (σ 22 ) to initiate transcription of the alginate biosynthetic operon.    Results  In the current study, we mapped the  mucE  transcriptional start site, and determined that P  mucE   activity was dependent on AlgU. Additionally, the presence of triclosan and sodium dodecyl sulfate was shown to cause an increase in P  mucE   activity. It was observed that  mucE -mediated mucoidy in CF isolates was dependent on both the size of MucA and the genotype of  algU . We also performed shotgun proteomic analysis with cell lysates from the strains PAO1, VE2 (PAO1 with constitutive expression of  mucE ) and VE2Δ algU  (VE2 with in-frame deletion of  algU ). As a result, we identified nine  algU -dependent and two  algU -independent proteins that were affected by overexpression of MucE.    Conclusions  Our data indicates there is a positive feedback regulation between MucE and AlgU. Furthermore, it seems likely that MucE may be part of the signal transduction system that senses certain types of cell wall stress to  P. aeruginosa .

Expression of mucoid induction factor MucE is dependent upon the alternate sigma factor AlgU in Pseudomonas aeruginosa