Abstract
Species interactions drive evolution while evolution shapes these interactions. The resulting eco-evolutionary dynamics, their outcomes and their repeatability depend on how adaptive mutations available to community members affect fitness and ecologically relevant traits. However, the diversity of adaptive mutations is not well characterized, and we do not know how this diversity is affected by the ecological milieu. Here we use barcode lineage tracking to address this gap in a competitive mutualism between the yeast Saccharomyces cerevisiae and the alga Chlamydomonas reinhardtii. We find that yeast has access to many adaptive mutations with diverse ecological consequences, in particular, those that increase and reduce the yields of both species. The presence of the alga does not change which mutations are adaptive in yeast (i.e., there is no fitness trade-off for yeast between growing alone or with alga), but rather shifts selection to favor yeast mutants that increase the yields of both species and make the mutualism stronger. Thus, in the presence of the alga, adaptations contending for fixation in yeast are more likely to enhance the mutualism, even though cooperativity is not directly favored by natural selection in our system. Our results demonstrate that ecological interactions not only alter the trajectory of evolution but also dictate its repeatability; in particular, weak mutualisms can repeatably evolve to become stronger.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Updated paper in response to reviewer's comments. * New data for Figure 1 * New analyses of the heuristic method for calling adapted lineages * Model showing that high-K/low-r mutations can be favored by selection * Various clarifications and streamlining throughout the text.
↵1 This number is larger than 0.18 expected based on the yeast mutation rate, but the difference is not statistically significant (P = 0.08, t-test, expected μ = 0.18).
↵2 This is confirmed by the fact that we find two mutations at driver loci in the neutral clones (see Figure S16 and Table S2).
