Antagonism between killer yeast strains as an experimental model for biological nucleation dynamics

Antagonistic interactions are widespread in the microbial world and affect microbial evolutionary dynamics. Natural microbial communities often display spatial structure, which affects biological interactions, but much of what we know about microbial antagonism comes from laboratory studies of well-mixed communities. To overcome this limitation, we manipulated two killer strains of the budding yeast Saccharomyces cerevisiae, expressing different toxins, to independently control the rate at which they released their toxins. We developed mathematical models that predict the experimental dynamics of competition between toxin-producing strains in both well-mixed and spatially structured populations. In both situations, we experimentally verified theory's prediction that a stronger antagonist can invade a weaker one only if the initial invading population exceeds a critical frequency or size. Finally, we found that toxin-resistant cells and weaker killers arose in spatially structured competitions between toxin-producing strains, suggesting that adaptive evolution can affect the outcome of microbial antagonism in spatial settings.

Automated summary

Antagonistic interactions are common in the microbial world, impacting microbial evolutionary dynamics. Spatial structure in natural microbial communities affects biological interactions. Experimental and theoretical findings show that a stronger antagonist can only invade a weaker one if the initial invading population exceeds a critical frequency or size. Spatially structured competitions between toxin-producing strains can lead to the emergence of toxin-resistant cells and weaker killers, suggesting that adaptive evolution plays a role in microbial antagonism outcomes in spatial settings.