The evolutionary ecology of fungal killer phenotypes.

Ecological interactions influence evolutionary dynamics by selecting upon fitness variation within species. Antagonistic interactions often promote genetic and species diversity, despite the inherently suppressive effect they can have on the species experiencing them. A central aim of evolutionary ecology is to understand how diversity is maintained in systems experiencing antagonism. In this review, we address how certain single-celled and dimorphic fungi have evolved allelopathic killer phenotypes that engage in antagonistic interactions. We discuss the evolutionary pathways to the production of lethal toxins, the functions of killer phenotypes and the consequences of competition for toxin producers, their competitors and toxin-encoding endosymbionts. Killer phenotypes are powerful models because many appear to have evolved independently, enabling across-phylogeny comparisons of the origins, functions and consequences of allelopathic antagonism. Killer phenotypes can eliminate host competitors and influence evolutionary dynamics, yet the evolutionary ecology of killer phenotypes remains largely unknown. We discuss what is known and what remains to be ascertained about killer phenotype ecology and evolution, while bringing their model system properties to the reader's attention.

Infection by dsRNA viruses is associated with enhanced sporulation efficiency in Saccharomyces cerevisiae.

Upon starvation diploid cells of the facultative sexual yeast Saccharomyces cerevisiae undergo sporulation, forming four metabolically quiescent and robust haploid spores encased in a degradable ascus. All endosymbionts, whether they provide net benefits or costs, utilize host resources; in yeast, this should induce an earlier onset of sporulation. Here, we tested whether the presence of endosymbiotic dsRNA viruses (M satellite and L-A helper) correspond with higher sporulation rate of their host, S. cerevisiae. We find that S. cerevisiae hosting both the M and L-A viruses (so-called "killer yeasts") have significantly higher sporulation efficiency than those without. We also found that the removal of the M virus did not reduce sporulation frequency, possibly because the L-A virus still utilizes host resources with and without the M virus. Our findings indicate that either virulent resource use by endosymbionts induces sporulation, or that viruses are spread more frequently to sporulating strains. Further exploration is required to distinguish cause from effect.