Mutations in the mucA gene of Pseudomonas aeruginosa promote disease exacerbation.

The mucA gene is a major genetic determinant of mucoid conversion in Pseudomonas aeruginosa isolated from patients with cystic fibrosis (CF) and represents a frequent hotspot for adaptive mutations. Although the role of the mucA gene in pathogen adaptation and virulence has been progressively elucidated, a comprehensive and systematic synthesis of its emerging functions and regulatory networks remains lacking. Here, we summarize current advances in the study of mucA, including its evolutionary origin, structural and functional characteristics, regulatory role in alginate biosynthesis, its mutation-associated pathogenic effects, and emerging strategies to studying or targeting mucA-deficient strains. Overall, this review highlights mucA as an important component of stress response networks in P. aeruginosa and summarizes current evidence that may inform future studies on risk stratification in chronic infections.