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. 2019 Mar 19;116(14):6525–6527. doi: 10.1073/pnas.1902734116

Fig. 1.

Fig. 1.

Speculative and simplified model of P. aeruginosa evolution in the CF lung (no. 1). The CF lung is initially colonized by P. aeruginosa that has wild-type (WT) Las, Rhl, and PQS QS systems, leading to high concentrations of all AIs (no. 2). Over time, LasR− strains evolve, possibly due to the selection for cheats that utilize the public good of the WT strain. As the LasR− cells increase in frequency, concentrations of AIs decrease (no. 3). LasR− cheats can regain functionality of the Rhl QS system by mutation of mexT. The LasR− and MexT− strains are able to produce proteases, C4-HSL, and PQS, but not N-3OC12-HSL (no. 4). The Rhl-activated strains can themselves be cheated on by null mutations to the PQS system. All of these strain phenotypes have been observed in clinical isolates, although the mutations underpinning them are not always understood. We also expect that each of these morphotypes can coexist in an infected lung due to spatial heterogeneity. RhlR− strains do not emerge as cheats because they have a fitness defect when growing in the presence of the reprogrammed LasR mutants with functioning Rhl systems. This also represents one evolutionary pathway, and we expect that there are other targets of selection that can lead to similar P. aeruginosa morphotypes.