Spatial population expansion promotes the evolution of cooperation in an experimental Prisoner's Dilemma

Cooperation is ubiquitous in nature, but explaining its existence remains a central interdisciplinary challenge. Cooperation is most difficult to explain in the Prisoner's Dilemma game, where cooperators always lose in direct competition with defectors despite increasing mean fitness. Here we demonstrate how spatial population expansion, a widespread natural phenomenon, promotes the evolution of cooperation. We engineer an experimental Prisoner's Dilemma game in the budding yeast Saccharomyces cerevisiae to show that, despite losing to defectors in nonexpanding conditions, cooperators increase in frequency in spatially expanding populations. Fluorescently labeled colonies show genetic demixing of cooperators and defectors, followed by increase in cooperator frequency as cooperator sectors overtake neighboring defector sectors. Together with lattice-based spatial simulations, our results suggest that spatial population expansion drives the evolution of cooperation by (1) increasing positive genetic assortment at population frontiers and (2) selecting for phenotypes maximizing local deme productivity. Spatial expansion thus creates a selective force whereby cooperator-enriched demes overtake neighboring defector-enriched demes in a "survival of the fastest". We conclude that colony growth alone can promote cooperation and prevent defection in microbes. Our results extend to other species with spatially restricted dispersal undergoing range expansion, including pathogens, invasive species, and humans

Tissue signals imprint ILC2 identity with anticipatory function.

Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25-, IL-33-receptor-, and TSLP-receptor-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18. Tissue ILC2 subsets were unaltered in number and expression in germ-free mice, suggesting that endogenous, tissue-derived signals drive the maturation of ILC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life

2v8_NoWeighingDispersal

Simulations were ran with expansion-collision dynamics and the initial cell-cell distance equals 2 and the assumption of weighted dispersal was relaxed

cooperation1cdDVD_deterministic_evenlydistributed_rareinvasion

Simulation code for rare invasion of a single cooperator or a single defector with expansion-collision dynamics

2v7_NoWeighingDispersal

Simulations were ran with expansion-collision dynamics and the initial cell-cell distance equals 1 and the assumption of weighted dispersal was relaxed

Data from: Microbial expansion-collision dynamics promote cooperation and coexistence on surfaces

Microbes colonizing a surface often experience colony growth dynamics characterized by an initial phase of spatial clonal expansion followed by collision between neighboring colonies to form potentially genetically heterogeneous boundaries. For species with life cycles consisting of repeated surface colonization and dispersal, these spatially-explicit “expansion-collision dynamics” generate periodic transitions between two distinct selective regimes, “expansion competition” and “boundary competition”, each one favoring a different growth strategy. We hypothesized that this dynamic could promote stable coexistence of expansion- and boundary-competition specialists by generating time-varying, negative frequency-dependent selection that insulates both types from extinction. We tested this experimentally in budding yeast by competing an exo-enzyme secreting “cooperator” strain (expansion-competition specialists) against non-secreting “defectors” (boundary-competition specialists). As predicted, we observed cooperator-defector coexistence or cooperator dominance with expansion-collision dynamics, but only defector dominance otherwise. Also as predicted, the steady-state frequency of cooperators was determined by colonization density (the average initial cell-cell distance) and cost of cooperation. Lattice-based spatial simulations give good qualitative agreement with experiments, supporting our hypothesis that expansion-collision dynamics with costly public goods production is sufficient to generate stable cooperator-defector coexistence. This mechanism may be important for maintaining public-goods cooperation-and-conflict in microbial pioneer species living on surfaces

The Genetic Signature of Conditional Expression

Conditionally expressed genes have the property that every individual in a population carries and transmits the gene, but only a fraction, φ, expresses the gene and exposes it to natural selection. We show that a consequence of this pattern of inheritance and expression is a weakening of the strength of natural selection, allowing deleterious mutations to accumulate within and between species and inhibiting the spread of beneficial mutations. We extend previous theory to show that conditional expression in space and time have approximately equivalent effects on relaxing the strength of selection and that the effect holds in a spatially heterogeneous environment even with low migration rates among patches. We support our analytical approximations with computer simulations and delineate the parameter range under which the approximations fail. We model the effects of conditional expression on sequence polymorphism at mutation–selection–drift equilibrium, allowing for neutral sites, and show that sequence variation within and between species is inflated by conditional expression, with the effect being strongest in populations with large effective size. As φ decreases, more sites are recruited into neutrality, leading to pseudogenization and increased drift load. Mutation accumulation diminishes the degree of adaptation of conditionally expressed genes to rare environments, and the mutational cost of phenotypic plasticity, which we quantify as the plasticity load, is greater for more rarely expressed genes. Our theory connects gene-level relative polymorphism and divergence with the spatial and temporal frequency of environments inducing gene expression. Our theory suggests that null hypotheses for levels of standing genetic variation and sequence divergence must be corrected to account for the frequency of expression of the genes under study