Abstract
BackgroundEvolutionary arms race plays a major role in shaping biological diversity. In microbial systems, competition often involves chemical warfare and the production of bacteriocins, narrow-spectrum toxins aimed at killing closely related strains by forming pores in their target’s membrane or by degrading the target’s RNA or DNA. Although many empirical and theoretical studies describe competitive exclusion of bacteriocin-sensitive strains by producers of bacteriocins, the dynamics among producers are largely unknown.Methodology/Principal findingsWe used a reporter-gene assay to show that the bacterial response to bacteriocins’ treatment mirrors the inflicted damage Potent bacteriocins are lethal to competing strains, but at sublethal doses can serve as strong inducing agents, enhancing their antagonists’ bacteriocin production. In contrast, weaker bacteriocins are less toxic to their competitors and trigger mild bacteriocin expression. We used empirical and numerical models to explore the role of cross-induction in the arms race between bacteriocin-producing strains. We found that in well-mixed, unstructured environments where interactions are global, producers of weak bacteriocins are selectively advantageous and outcompete producers of potent bacteriocins. However, in spatially structured environments, where interactions are local, each producer occupies its own territory, and competition takes place only in “no man’s lands” between territories, resulting in much slower dynamics.Conclusion/SignificanceThe models we present imply that producers of potent bacteriocins that trigger a strong response in neighboring bacteriocinogenic strains are doomed, while producers of weak bacteriocins that trigger a mild response in bacteriocinogenic strains flourish. This counter-intuitive outcome might explain the preponderance of weak bacteriocin producers in nature. However, the described scenario is prolonged in spatially structured environments thus promoting coexistence, allowing migration and evolution, and maintaining bacterial diversity.
Highlights
Species that comprise highly diverse communities are often engaged in a fierce arms race over resources and space
The leading antibiotics used in the bacteria and archaea world are bacteriocins [3] – proteinaceous toxins that enable their producing organisms to defend their habitat against invaders, limit the advance of neighboring cells [4] or invade an established bacterial community [5,6]
All colicin producing strains and their isogenic host lacking the colicin-encoding vector (Table 1) were induced to produce colicins, but not before we demonstrated that the treatment we applied prompt similar expression in the different colicinogenic strains (Table S1)
Summary
Species that comprise highly diverse communities are often engaged in a fierce arms race over resources and space. To overcome their adversaries, species, large and small, use every weapon in their arsenal including secondary metabolites, extracellular enzymes, or antibiotics, [1,2]. Most of the characterized colicins (and bacteriocins) make pores in their antagonists’ inner membrane, while the others degrade either the DNA or RNA of the target cell [7]. Competition often involves chemical warfare and the production of bacteriocins, narrow-spectrum toxins aimed at killing closely related strains by forming pores in their target’s membrane or by degrading the target’s RNA or DNA. Many empirical and theoretical studies describe competitive exclusion of bacteriocin-sensitive strains by producers of bacteriocins, the dynamics among producers are largely unknown
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