Pseudomonas aeruginosa in cystic fibrosis: role of mucC in the regulation of alginate production and stress sensitivity

Abstract

Alginate production inPseudomonas aeruginosaand the associated mucoid phenotype of isolates from cystic fibrosis patients are under the control of thealgU mucABCDcluster. This group of genes encodes AlgU, theP. aeruginosaequivalent of the extreme heat shock σ factor σEin Gram-negative bacteria, the AlgU-cognate anti-σ factor MucA, the periplasmic protein MucB and a serine protease homologue, MucD. WhilemucA, mucBormucDact as negative regulators of AlgU, the function ofmucCis not known. In this study the role ofmucCinP. aeruginosaphysiology and alginate production has been addressed. Insertional inactivation ofmucCin the wild-typeP. aeruginosastrain PAO1 did not cause any overt effects on alginate synthesis. However, it affected growth ofP. aeruginosaunder conditions of combined elevated temperature and increased ionic strength or osmolarity. inactivation ofmucCinmucAormucBmutant backgrounds resulted in a mucoid phenotype when the cells were grown under combined stress conditions of elevated temperature and osmolarity. Each of the stress factors tested separately did not cause comparable effects. The combined stress factors were not sufficient to cause phenotypically appreciable enhancement of alginate production inmucAormucBmutants unlessmucCwas also inactivated. These findings support a negative regulatory role ofmucCin alginate production byP. aeruginosa,indicate additive effects ofmucgenes in the regulation of mucoidy in this organism and suggest that multiple stress signals and recognition systems participate in the regulation ofalgu-dependent functions.