We showed that the Phc quorum sensing system required for the virulence of the ancestral bacterium was reconfigured to improve intracellular infection of root nodules induced by evolved Ralstonia. A single mutation in either the PhcB autoinducer synthase or the PhcQ regulator of the sensory cascade tuned the kinetics of activation of the central regulator PhcA in response to cell density so that the minimal stimulatory concentration of autoinducers needed for a given response was increased. Here, ACER3 is linked to infection.