Mucoid Pseudomonas aeruginosa and cystic fibrosis: the role of mutations in muc loci

Abstract

Mucoid alginate-producing mutants of Pseudomonas aeruginosa are major pathogens in debilitating chronic pulmonary infections in patients with cystic fibrosis. The mucoid phenotype results from alginate biosynthesis whose genes are arranged in at least three chromosomal loci. Structural genes are located at the 34-min region and regulatory genes at 9 min. A third cluster at the 70 min region contains muc mutations which affect transcription of a key structural gene, algD, in response to environmental stimuli. Control of mucoidy includes bacterial signal transduction systems, histone-like elements controlling nucleoid structure and, possibly, factors affecting superhelicity. Thus, the control of mucoidy in P. aeruginosa has become one of the focal systems for analysis of how bacterial pathogens adapt to the host environment.