Abstract

Allelopathic interactions mediated by bacteriocins production serve microorganisms in the never-ending battle for resources and living space. Competition between the bacteriocin producer and sensitive populations results in the exclusion of one or the other depending on their initial frequencies, the structure of their habitat, their community density and their nutrient availability. These interactions were extensively studied in bacteriocins produced by Escherichia coli, the colicins. In spatially structured environments where interactions are local, colicin production has been shown to be advantageous to the producer population, allowing them to compete even when initially rare. Yet, in a well-mixed, unstructured environment where interactions are global, rare producer populations cannot invade a common sensitive population. Here we are showing, through an experimental model, that colicin-producers can outcompete sensitive and producer populations when the colicin production rates are enhanced. In fact, colicin production rates were proportional to the producer competitive fitness and their overall success in out-competing opponents when invading at very low initial frequencies. This ability of rare populations to invade established communities maintains diversity and allows the dispersal of beneficial traits.

Highlights

  • Microbial communities’ continuous competition for shared limited resources and space is often resolved by the production of toxins [1]

  • In a previous study we explored allelopathic interaction using colicins, bacteriocins produced by Escherichia coli

  • The mode of action of all four colicins used in this study is similar; they all kill their competitors by DNA degradation [22,30], yet, they vary in their colicin-expression rate (Table 2)

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Summary

Introduction

Microbial communities’ continuous competition for shared limited resources and space is often resolved by the production of toxins [1]. Coexistence of toxin-producer and susceptible, non-producer populations has been studied in many bacteria and yeast communities [2]. Competition between toxin producer and sensitive populations results in the exclusion of one or the other, depending on their initial frequencies [3,4], the structure of their habitat [5], the community density [6] and nutrient availability [7]. In spatially structured environments, where cells are sessile and interactions are local, bacteriocin-producing colonies kill neighboring sensitive cells and are rewarded by an increase of available resources in their vicinity [5]. The producer competitive advantage is reduced either at low densities, probably because of reduced interactions [6], or when populations are clonally segregated, and susceptible species can coexist or even outcompete producers [10]. Killing is costly and a lack of competition with sensitive cells reduces the fitness of the producers to a point where they are out-competed by non-producer, sensitive cells [5]

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