Strong spatial population structure shapes the temporal coevolutionary dynamics of costly female preference and male display

Female mating preferences for exaggerated male display traits are commonplace. Yet, comprehensive understanding of the evolution and persistence of costly female preference through indirect (Fisherian) selection in finite populations requires some explanation for the persistence of additive genetic variance (Va) underlying sexual traits, given that directional preference is expected to deplete Va in display and hence halt preference evolution. However, the degree to which Va, and hence preference-display coevolution, may be prolonged by spatially variable sexual selection arising solely from limited gene flow and genetic drift within spatially structured populations has not been examined. Our genetically and spatially explicit model shows that spatial population structure arising in an ecologically homogeneous environment can facilitate evolution and long-term persistence of costly preference given small subpopulations and low dispersal probabilities. Here, genetic drift initially creates spatial variation in female preference, leading to persistence of Va in display through migration-bias of genotypes maladapted to emerging local sexual selection, thus fuelling coevolution of costly preference and display. However, costs of sexual selection increased the probability of subpopulation extinction, limiting persistence of high preference-display genotypes. Understanding long-term dynamics of sexual selection systems therefore requires joint consideration of coevolution of sexual traits and metapopulation dynamics.

CRISPR-based herd immunity can limit phage epidemics in bacterial populations

Herd immunity, a process in which resistant individuals limit the spread of a pathogen among susceptible hosts has been extensively studied in eukaryotes. Even though bacteria have evolved multiple immune systems against their phage pathogens, herd immunity in bacteria remains unexplored. Here we experimentally demonstrate that herd immunity arises during phage epidemics in structured and unstructured Escherichia coli populations consisting of differing frequencies of susceptible and resistant cells harboring CRISPR immunity. In addition, we develop a mathematical model that quantifies how herd immunity is affected by spatial population structure, bacterial growth rate, and phage replication rate. Using our model we infer a general epidemiological rule describing the relative speed of an epidemic in partially resistant spatially structured populations. Our experimental and theoretical findings indicate that herd immunity may be important in bacterial communities, allowing for stable coexistence of bacteria and their phages and the maintenance of polymorphism in bacterial immunity.