RT Journal Article SR Electronic T1 Competition in biofilms between Pseudomonas aeruginosa cystic fibrosis isolates is driven by R-pyocins JF bioRxiv FD Cold Spring Harbor Laboratory SP 264580 DO 10.1101/264580 A1 Olubukola Oluyombo A1 Stephen P. Diggle A1 Christopher N. Penfold YR 2018 UL http://biorxiv.org/content/early/2018/02/13/264580.abstract AB Pseudomonas aeruginosa is an opportunistic pathogen responsible for a number of different human infections and is the leading cause of morbidity and mortality in cystic fibrosis (CF) patients. P. aeruginosa infections are difficult to treat due to a number of antibiotic resistance mechanisms and the organisms propensity to form multicellular biofilms. Epidemic strains of P. aeruginosa often displace and dominate other strains within the lungs of individual CF patients, but how they achieve this is poorly understood. One of the ways strains can compete with each other is by producing chromosomally encoded bacteriocins, called pyocins. Three major classes of pyocin have been identified in P. aeruginosa: soluble pyocins (S-types) and tailocins (R- and F-types). In this study, we investigated the distribution of S- and R-type pyocins in 24 clinical strains isolated from individual CF patients and then focused on understanding their roles on inter-strain competition. We found that (i) each strain produced only one R-pyocin type, but the number of S-pyocins varied between strains; (ii) R-pyocins were crucial for strain dominance during competition assays in both planktonic cultures and within biofilms; (iii) purified R-pyocins demonstrated significant antimicrobial activity against established biofilms. Our work provides clear support for the role played by R-pyocins in competition between P. aeruginosa strains and may help explain why certain strains and lineages of P. aeruginosa displace others during CF lung infection. Furthermore, we demonstrate the potential of exploiting R-pyocins for therapeutic gains in an era when antibiotic resistance is a global concern.