Clinical isolates of Pseudomonas aeruginosa from patients with cystic fibrosis (CF) often have mutations that affect two-component systems (TCSs) that sense and respond to environmental stimuli. Cao et al. found that mutations in CF-adapted P. aeruginosa strains that affected the sensor histidine kinase BfmS promoted phenotypic changes associated with chronic infection by causing the loss of BfmS-mediated inhibition of its downstream= effector, BfmR. Under these conditions, GtrS, a sensor histidine kinase from a different TCS, promoted BfmR activity in the presence of glucose, which is abundant in the CF lung. Thus, mutations that affect a TCS may contribute to host adaptation both directly by dysregulating a cognate TCS and indirectly by enabling aberrant cross-talk between noncognate TCSs.
The study was published in Science Signaling entitled “Mutation-induced remodeling of the BfmRS two-component system in Pseudomonas aeruginosa clinical isolates” on November 3 and was highlighted on the homepage of Science. CAO Qiao, doctoral supervisor at Northwestern University and associate researcher at Shanghai Institute of Material Medica of Chinese Academy of Sciences, is the first author; LAN Lefu, doctoral supervisor at University of Chinese Academy of Sciences and associate researcher at Shanghai Institute of Material Medica of Chinese Academy of Sciences, is the corresponding author.
