GEE Seminar - Prof Michael Turelli, University of California, Davis

Academic Host: Ziheng Yang
Abstract: Cytoplasmic incompatibility (CI) is the most common reproductive manipulation produced by Wolbachia, obligately intracellular alphaproteobacteria that infect roughly half of all insect species. Once infection frequencies within host populations approach 10%, intense CI can drive Wolbachia to near fixation within 10 generations. However, natural selection among Wolbachiavariants within individual host populations does not favor enhanced CI. Indeed, variants that do not cause CI, but increase host fitness or are more reliably maternally transmitted, are expected to spread –– if infected females remain protected from CI (Turelli 1994 Evolution 48:1500–1513). Nevertheless, roughly half of analyzed Wolbachia infections cause detectable CI. Why? The frequency and persistence of CI are more plausibly explained by preferential spread to new host species (“clade selection”) rather than by natural selection among variants within host populations. CI-causing Wolbachia lineages preferentially spread into new host species because: 1) CI increases equilibrium Wolbachia frequencies within host populations, and 2) CI-causing variants can remain at high frequencies within populations even when conditions change so that initially beneficial Wolbachia infections become harmful. An epidemiological model describing Wolbachia acquisition and loss by host species and the loss of CI-induction within Wolbachialineages yields simple expressions for the incidence of Wolbachia infections and the fraction of those infections causing CI. Supporting a determinative role for differential interspecific spread in maintaining CI, many Wolbachia infections were recently acquired by their host species, many show evidence for contemporary spatial spread or retreat, and rapid evolution of CI-inducing loci, especially degradation, is common.