Abstract
Chronic respiratory complications in cystic fibrosis, compounded by recurring infections with mucoid Pseudomonas aeruginosa and the associated inflammation, are the primary cause of high mortality in this inheritable disease. Since the conversion of P. aeruginosa into the exopolysaccharide alginate overproducing strains plays a critical role in the establishment of chronic infection, studies are directed towards understanding the processes underlying this phenomenon. The genes (algU, mucA, and mucB) and genetic alterations responsible for conversion to mucoidy have been recently characterized. The mutations leading to the emergence of mucoid strains are superimposed on a regulatory system with elements that resemble those controlling other aspects of bacterial developmental physiology.
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