ArticleMolecular microbiology2007
Growth phenotypes of Pseudomonas aeruginosa lasR mutants adapted to the airways of cystic fibrosis patients.
Article in Molecular microbiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers.
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Who cites it
217 citing papers in PubMed.
- Pseudomonas aeruginosa phenotypes associated with eradication failure in children with cystic fibrosis.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014Trial
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- Loss of LasR function leads to decreased repression ofJournal of bacteriology · 2025Article
- Co-culture biofilm patterns among different Pseudomonas aeruginosa clones from cystic fibrosis patients.Biofilm · 2025Article
- Antibiotic-ResistantMicroorganisms · 2025Review
- Disruption ofMicrobiology (Reading, England) · 2025Article
- Analysing theFrontiers in cellular and infection microbiology · 2025Review
157 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors.
Funding
Abstract
The opportunistic pathogen Pseudomonas aeruginosa undergoes genetic change during chronic airway infection of cystic fibrosis (CF) patients. One common change is a mutation inactivating lasR, which encodes a transcriptional regulator that responds to a homoserine lactone signal to activate expression of acute virulence factors. Colonies of lasR mutants visibly accumulated the iridescent intercellular signal 4-hydroxy-2-heptylquinoline. Using this colony phenotype, we identified P. aeruginosa lasR mutants that emerged in the airway of a CF patient early during chronic infection, and during growth in the laboratory on a rich medium. The lasR loss-of-function mutations in these strains conferred a growth advantage with particular carbon and nitrogen sources, including amino acids, in part due to increased expression of the catabolic pathway regulator CbrB. This growth phenotype could contribute to selection of lasR mutants both on rich medium and within the CF airway, supporting a key role for bacterial metabolic adaptation during chronic infection. Inactivation of lasR also resulted in increased beta-lactamase activity that increased tolerance to ceftazidime, a widely used beta-lactam antibiotic. Loss of LasR function may represent a marker of an early stage in chronic infection of the CF airway with clinical implications for antibiotic resistance and disease progression.
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