Disrupting Pseudomonas aeruginosa quorum sensing
Many clinically relevant bacterial pathogens (e.g. Pseudomonas aeruginosa) use chemical signals to communicate with one another as a precursor to initiating infections and/or biofilm formation. Otherwise known as quorum sensing, this process enables pathogens to restrict the expression of specific genes until a population capable of overwhelming the host defences is reached. Due to the important role of quorum sensing in bacterial pathogenesis, the disruption of this system (quorum quenching) is a promising antimicrobial strategy.
Quorum sensing involves the synthesis, secretion and detection of chemical signals, termed autoinducers. Disrupting any one of these steps can inhibit quorum sensing. P. aeruginosa uses two N-acyl-homoserine lactone (AHL) autoinducers for quorum sensing. Previous research has identified a number of small molecule inhibitors with picomolar affinities for two enzymes involved in AHL synthesis. However, the effects of these inhibitors on P. aeruginosa quorum sensing were not tested. The aim of this project was to generate gene deletions of these targets in P. aeruginosa and characterise their effects.
|Date||Tuesday, 4 December 2018|
|Time||12:00pm - 1:00pm|
|Event Category||Health Sciences|
|Location||Biochemistry Seminar Room 231|