Madeline Mei from Diggle lab will present her work on R-pyocins and competition between Pseudomonas aeruginosa strains

Summary:

R-Pyocin-mediated killing between Pseudomonas aeruginosa strains isolated from cystic fibrosis lungs

Pseudomonas aeruginosa (Pa) is a prevalent Gram-negative opportunistic pathogen found in a number of infections; however, it is a major problem in lung infections of individuals with cystic fibrosis (CF). It is believed that one strain of Pa takes over and diversifies over the course of these chronic lung infections, but the mechanism for this is poorly understood. R-type pyocins are narrow spectrum, phage tail-like bacteriocins, specifically produced by Pa to kill other strains of Pa. Current studies have shown that R-type pyocins can play a role in intra-species competition due to the production of various types (types 1-5) of R-pyocins, as each strain produces only one of the five R-pyocin types. 

Using our “biobank” of whole populations of Pa from CF patients, we found that (i) populations collected from a single sputum sample produce the same R-pyocin type; (ii) populations from the same sputum sample exhibit diversity in susceptibility to pyocins of other isolates of Pa; (iii) differential susceptibility of CF isolates to R-pyocins is due to differences in lipopolysaccharide (LPS). Our work is a step towards understanding how intra-strain competition via pyocins can affect the dynamics of evolved, diverse Pa populations.