The Pseudomonas aeruginosa quinolone signal molecule overcomes the cell density‐dependency of the quorum sensing hierarchy, regulates rhl‐dependent genes at the onset of stationary phase and can be produced in the absence of LasR

摘要: In Pseudomonas aeruginosa, diverse exoproduct virulence determinants are regulated via N-acylhomoserine lactone-dependent quorum sensing. Here we show that 2-heptyl-3-hydroxy-4(1H)-quinolone (PQS) is also an integral component of the sensing circuitry and required for production rhl-dependent exoproducts at onset stationary phase. Analysis spent P. aeruginosa culture supernatants revealed PQS produced end exponential phase in parent strain late a lasR mutant. Mutants defective both (pqsR-) response (pqsE-) substantially reduced levels but retained wild-type N-butanoyl homoserine lactone (C4-HSL) levels. wild type, provision exogenous time inoculation significantly increased PA-IL lectin, pyocyanin elastase during early promoted biofilm formation. Exogenous not derivatives lacking 3-hydroxy group overcame cell density growth phase-dependent exoproducts. transcriptional post-transcriptional repression lecA (which codes lectin) mediated negative regulators MvaT RsmA respectively. Increased expression presence can be explained partially by increases RhlR, RpoS C4-HSL A refined model presented.