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1.
Proc Natl Acad Sci U S A ; 98(25): 14613-8, 2001 Dec 04.
Article in English | MEDLINE | ID: mdl-11724939

ABSTRACT

The human opportunistic pathogen Pseudomonas aeruginosa strain PA14 infects both plants and animals. Previously, using plants to screen directly for P. aeruginosa virulence-attenuated mutants, we identified a locus, pho34B12, relevant in mammalian pathogenesis. Here, nonsense point mutations in the two opposing ORFs identified in the pho34B12 locus revealed that one of them, mvfR (multiple virulence factor Regulator), is able to control all of the phenotypes that mutant phoA34B12 displays. Both genetic and biochemical evidence demonstrate that the mvfR gene encodes a LysR-like transcriptional factor that positively regulates the production of elastase, phospholipase, and of the autoinducers, 3oxo-dodecanoyl homoserine lactone (PAI I) and 2-heptyl-3-hydroxy-4-quinolone (PQS), as well as the expression of the phnAB operon, involved in phenazine biosynthesis. We demonstrate that the MvfR protein is membrane-associated and acts as a transcriptional activator until cells reach stationary phase, when a unique negative feedback mechanism is activated to signal the down-regulation of the MvfR protein. This work reveals an unprecedented virulence mechanism of P. aeruginosa and identifies a unique indispensable player in the P. aeruginosa quorum-sensing cascade.


Subject(s)
Genes, Bacterial , Pseudomonas aeruginosa/genetics , Pseudomonas aeruginosa/pathogenicity , Animals , Bacterial Proteins/genetics , Bacterial Proteins/metabolism , Codon, Nonsense , Escherichia coli/genetics , Feedback , Humans , Open Reading Frames , Operon , Phenotype , Point Mutation , Pseudomonas aeruginosa/metabolism , Transcription Factors/genetics , Virulence/genetics
2.
Proc Natl Acad Sci U S A ; 97(16): 8815-21, 2000 Aug 01.
Article in English | MEDLINE | ID: mdl-10922040

ABSTRACT

By exploiting the ability of Pseudomonas aeruginosa to infect a variety of vertebrate and nonvertebrate hosts, we have developed model systems that use plants and nematodes as adjuncts to mammalian models to help elucidate the molecular basis of P. aeruginosa pathogenesis. Our studies reveal a remarkable degree of conservation in the virulence mechanisms used by P. aeruginosa to infect hosts of divergent evolutionary origins.


Subject(s)
Arabidopsis/microbiology , Pseudomonas aeruginosa/pathogenicity , Virulence , Animals , Biological Evolution , Burns/microbiology , Mice , Plants
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