Bacteria can evolve quickly, a skill that proves useful in ever-changing environments. For example, individuals in many bacterial species can start to work together under certain circumstances; this ability is underpinned by a system called quorum sensing, which allows cells to detect nearby conspecifics. However, species of harmful bacteria often lose their quorum sensing abilities when they infect humans. This is the case for Pseudomonas aeruginosa, which normally lives in the soil but can also cause deadly conditions, especially in hospital settings.
Patients often carry P. aeruginosa with mutations that disable the quorum-sensing signal receptor LasR, a molecular actor that can switch on many other genes in a cell. People who are infected with P. aeruginosa strains carrying a damaged version of the lasR gene are typically more ill and less likely to recover. Why this is the case – and in fact, why genes associated with quorum sensing often lose function during infection – is still unclear.
To investigate this question, Mould et al. used laboratory evolution experiments and computer models of P. aeruginosa growth to understand how lasR mutant cells evolve. Differences in growth rates and ways to use resources (rather than changes in cell-to-cell interactions) best explained why lasR mutants become more successful. Further experiments narrowed down the molecular cascade required for the rise of lasR mutants, identifying a pathway that regulates how P. aeruginosa switches between different nutrient sources.
This work reveals a new connection between quorum sensing genes and nutrient regulation in bacterial cells. Loss of functional LasR changes the way that cells use nutrients, and thus will reshape how they interact with host cells and other bacteria. This insight could lead to better ways to predict the outcomes of bacterial infections and how to best treat them.