A spatial model of the evolution of quorum sensing regulating bacteriocin production

Like any form of cooperative behavior, quorum sensing (QS) inbacteria is potentially vulnerable to cheating, the occurrenceof individuals that contribute less but still profit from thebenefits provided by others. In this paper, we explore the evolutionarystability of QS as a regulatory mechanism of antibiotics productionin a spatially structured population, using cellular automaton(CA) modeling. QSg is supposed to regulate the excretion ofa bacteriocin (anticompetitor toxin) in a population of bacteriapolymorphic for the ability to produce and to be immune to thebacteriocin. Both the social interactions resulting from QSand the competitive interactions resulting from the bacteriocinexcretion are supposed to be only effective at the local scale,that is, restricted to the immediately neighboring cells. Thisimplies a rather diffuse kind of group selection. The CA modelis contrasted to a model assuming no spatial structure but withotherwise identical assumptions. Our analysis predicts thatQS as a regulatory mechanism of bacteriocin excretion is evolutionarilyunstable when the competitive interactions between bacteriocin-producing,resistant, and sensitive strains only involve closely relatedstrains which can share the signaling and responding genes involvedin QS. However, when the competition is between unrelated strainsand the QS alleles can only be carried by the bacteriocin-producingstrains, stable QS may evolve provided its costs are small andthe critical quorum threshold is neither too low nor too high.