Shuya Zhai, James Schafhauser, Geoffrey McKay, Dao Nguyen*, McGill University
Full manuscript: www.kon.org/urc/v13/zhai.html
Abstract: Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the cystic fibrosis transmembrane regulator (CFTR) gene. CF patients are more susceptible to opportunistic infections by different bacteria, and most importantly P. aeruginosa,which causes both acute and chronic infections because of its ability to secrete numerous virulent compounds and degradative enzymes. Expression of the virulent compounds is controlled by quorum sensing. The Pseudomonas Quinolone Signal system (PQS) is one of three quorum-sensing networks in P. aeruginosa. A study found that sub-inhibitory concentration of the cationic antimicrobial peptide (CAMP) colistin induced PQS overproduction in P. aeruginosa, but the exact mechanism remains elusive. It was also previously demonstrated that the gene PA5003 is required for P. aeruginosa to recognize and respond to the presence of the CAMPs (colistin). From a random mutagenesis screen conducted, our lab also demonstrated that loss of PA5003 led to reduced PQS expression. These observations led us to hypothesize that PA5003 is required for colistin-induced PQS over-production. In this study, we confirmed that colistin induced over-expression of pqsA, one of the PQSbiosynthesis genes, and demonstrated that PA5003 plays a role in the overexpression of pqsA induced by sub-inhibitory concentration of colistin.
Read the full manuscript: www.kon.org/urc/v13/zhai.html