Abstract
Tit-for-tat is a familiar principle from animal behavior: individuals respond in kind to being helped or harmed by others. Remarkably some bacteria appear to display tit-for-tat behavior, but how this evolved is not understood. Here we combine evolutionary game theory with agent-based modelling of bacterial tit-for-tat, whereby cells stab rivals with poisoned needles (the type VI secretion system) after being stabbed themselves. Our modelling shows tit-for-tat retaliation is a surprisingly poor evolutionary strategy, because tit-for-tat cells lack the first-strike advantage of preemptive attackers. However, if cells retaliate strongly and fire back multiple times, we find that reciprocation is highly effective. We test our predictions by competing Pseudomonas aeruginosa (a tit-for-tat species) with Vibrio cholerae (random-firing), revealing that P. aeruginosa does indeed fire multiple times per incoming attack. Our work suggests bacterial competition has led to a particular form of reciprocation, where the principle is that of strong retaliation, or ‘tits-for-tat’.
Highlights
Tit-for-tat is a familiar principle from animal behavior: individuals respond in kind to being helped or harmed by others
We recently reported a new version of this model[44], designed for the study of T6SS competition, in which cells can intoxicate neighbors by firing T6SS needles
We found that random constitutive firing of the T6SS can readily evolve in unarmed populations, provided that (i) weapon costs are not excessive and (ii) initial mixing provides enough interstrain contact
Summary
Tit-for-tat is a familiar principle from animal behavior: individuals respond in kind to being helped or harmed by others. We test our predictions by competing Pseudomonas aeruginosa (a tit-for-tat species) with Vibrio cholerae (random-firing), revealing that P. aeruginosa does fire multiple times per incoming attack. It has been shown that various stimuli can trigger counterattacks in P. aeruginosa strain PAO1, including incoming T6SS attacks from multiple bacterial species[23,27,28], conjugative T4SS pili[29], and membrane-disrupting antibiotics like polymyxin B29. P. aeruginosa appears to be responding to membrane perturbation, and a putative model is that this response is mediated post-transcriptionally via the TagQRST pathway. This signaling cascade leads to the localized phosphorylation of cytoplasmic Fha[1] proteins, and subsequent T6SS activation[31,32,33]. Understanding the evolution of T6SS regulation and retaliation is important, both for understanding bacterial warfare and as a distinct case in evolutionary biology
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