Lactonase Specificity Is Key to Quorum Quenching in Pseudomonas aeruginosa.

ABSTRACT: The human opportunistic pathogen Pseudomonas aeruginosa orchestrates the expression of many genes in a cell density-dependent manner by using quorum sensing (QS). Two acyl-homoserine lactones (AHLs) are involved in QS circuits and contribute to the regulation of virulence factors production, biofilm formation, and antimicrobial sensitivity. Disrupting QS, a strategy referred to as quorum quenching (QQ) can be achieved using exogenous AHL-degrading lactonases. However, the importance of enzyme specificity on quenching efficacy has been poorly investigated. Here, we used two lactonases both targeting the signal molecules N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C₁₂ HSL) and butyryl-homoserine lactone (C₄ HSL) albeit with different efficacies on C

SUBMITTER: Remy B 

PROVIDER: S-EPMC7193897 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature