The PqsE Active Site as a Target for Small Molecule Antimicrobial Agents against Pseudomonas aeruginosa.

ABSTRACT: The opportunistic pathogen Pseudomonas aeruginosa causes antibiotic-resistant, nosocomial infections in immuno-compromised individuals and is a high priority for antimicrobial development. Key to pathogenicity in P. aeruginosa are biofilm formation and virulence factor production. Both traits are controlled by the cell-to-cell communication process called quorum sensing (QS). QS involves the synthesis, release, and population-wide detection of signal molecules called autoinducers. We previously reported that the activity of the RhlR QS transcription factor depends on a protein-protein interaction with the hydrolase, PqsE, and PqsE catalytic activity is dispensable for this interaction. Nonetheless, the PqsE-RhlR interaction could be disrupted by the substitution of an active

SUBMITTER: Taylor IR 

PROVIDER: S-EPMC9454246 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature