The evolution of strategy in bacterial warfare via the regulation of bacteriocins and antibiotics

Bacteria inhibit and kill one another with a diverse array of compounds, including bacteriocins and antibiotics. These attacks are highly regulated, but we lack a clear understanding of the evolutionary logic underlying this regulation. Here, we combine a detailed dynamic model of bacterial competition with evolutionary game theory to study the rules of bacterial warfare. We model a large range of possible combat strategies based upon the molecular biology of bacterial regulatory networks. Our model predicts that regulated strategies, which use quorum sensing or stress responses to regulate toxin production, will readily evolve as they outcompete constitutive toxin production. Amongst regulated strategies, we show that a particularly successful strategy is to upregulate toxin production in response to an incoming competitor's toxin, which can be achieved via stress responses that detect cell damage (competition sensing). Mirroring classical game theory, our work suggests a fundamental advantage to reciprocation. However, in contrast to classical results, we argue that reciprocation in bacteria serves not to promote peaceful outcomes but to enable efficient and effective attacks.

Automated summary

Bacteria use a variety of compounds to inhibit and kill each other, and through evolution, bacteria can gain advantages by regulating toxin production, especially by increasing toxin production in response to competitors' toxins. Reciprocation in bacterial warfare serves to enable efficient and effective attacks, providing a fundamental advantage to reciprocation.