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

Like any form of cooperative behavior, quorum sensing (QS) in bacteria is potentially vulnerable to cheating, the occurrence of individuals that contribute less but still profit from the benefits provided by others. In this paper, we explore the evolutionary stability of QS as a regulatory mechanism of antibiotics production in a spatially structured population, using cellular automaton (CA) modeling. QSg is supposed to regulate the excretion of a bacteriocin (anticompetitor toxin) in a population of bacteria polymorphic for the ability to produce and to be immune to the bacteriocin. Both the social interactions resulting from QS and the competitive interactions resulting from the bacteriocin excretion are supposed to be only effective at the local scale, that is, restricted to the immediately neighboring cells. This implies a rather diffuse kind of group selection. The CA model is contrasted to a model assuming no spatial structure but with otherwise identical assumptions. Our analysis predicts that QS as a regulatory mechanism of bacteriocin excretion is evolutionarily unstable when the competitive interactions between bacteriocin-producing, resistant, and sensitive strains only involve closely related strains which can share the signaling and responding genes involved in QS. However, when the competition is between unrelated strains and the QS alleles can only be carried by the bacteriocin-producing strains, stable QS may evolve provided its costs are small and the critical quorum threshold is neither too low nor too high. Copyright 2007, Oxford University Press.