Bacteria are often thought of as simple, solitary organisms, but many species can coordinate their behavior as a group, a process called quorum sensing. When enough bacteria accumulate in one place, they release and detect small chemical signals that trigger collective behaviors, including the production of toxins and other factors that make infections difficult to treat.
Pseudomonas aeruginosa, a bacterium responsible for severe and often drug-resistant infections, particularly in people with cystic fibrosis or compromised immune systems, relies on quorum sensing to cause disease. A recent study published in the Journal of Bacteriology by the laboratories of Dr. Jon Paczkowski and Joe Wade in the Wadsworth Center’s Division of Genetics investigated how P. aeruginosa fine-tunes one of its key quorum-sensing receptors, a protein called RhlR. Rather than acting as a simple on/off switch, RhlR functions more like a dimmer, its activity is shaped both by the chemical signal it detects and by a partner protein called PqsE.
By engineering versions of RhlR with altered signal sensitivity, the researchers found that small changes in how well RhlR detects its signal can selectively rewire which genes get turned on, particularly those responsible for producing toxins. This is significant because novel drug therapies could be developed to inhibit RhlR, shutting down quorum sensing and rendering P. aeruginosa non-pathogenic.