作者: K. M. Sandoz , S. M. Mitzimberg , M. Schuster
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摘要: In a process termed quorum sensing, bacteria use diffusible chemical signals to coordinate cell density-dependent gene expression. the human pathogen Pseudomonas aeruginosa, sensing controls hundreds of genes, many which encode extracellular virulence factors. Quorum is required for P. aeruginosa in animal models. Curiously, sensing-deficient variants, most carry mutation encoding central regulator lasR, are frequently isolated from acute and chronic infections. The mechanism their emergence not known. Here we provide experimental evidence suggesting that these lasR mutants social cheaters cease production quorum-controlled factors take advantage by group. We detected an emerging subpopulation after ≈100 generations vitro evolution wild-type strain under culture conditions require growth. Under such conditions, appears impose metabolic burden on proliferating bacterial cell, because genes normally induced until cessation growth were highly expressed early growth, defined mutant showed when cocultured with parent strain. quorum-sensing-deficient variants certain environments therefore indicator high activity population as whole. It does necessarily indicate insignificant, has previously been suggested. Thus, novel antivirulence strategies aimed at disrupting communication may be particularly effective clinical settings.