Evolutionary trade-offs associated with loss of PmrB function in host-adapted Pseudomonas aeruginosa.

ABSTRACT: Pseudomonas aeruginosa colonises the upper airway of cystic fibrosis (CF) patients, providing a reservoir of host-adapted genotypes that subsequently establish chronic lung infection. We previously experimentally-evolved P. aeruginosa in a murine model of respiratory tract infection and observed early-acquired mutations in pmrB, encoding the sensor kinase of a two-component system that promoted establishment and persistence of infection. Here, using proteomics, we show downregulation of proteins involved in LPS biosynthesis, antimicrobial resistance and phenazine production in pmrB mutants, and upregulation of proteins involved in adherence, lysozyme resistance and inhibition of the chloride ion channel CFTR, relative to wild-type strain LESB65. Accordingly, pmrB mutants are susceptible to

SUBMITTER: Bricio-Moreno L 

PROVIDER: S-EPMC6035264 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature