Loss of cytoplasmic incompatibility and minimal fecundity effects explain relatively low Wolbachia frequencies in Drosophila mauritiana

Maternally transmitted Wolbachia bacteria infect about half of all insect species. Many Wolbachia cause cytoplasmic incompatibility (CI) and reduced egg hatch when uninfected females mate with infected males. Although CI produces a frequency‐dependent fitness advantage that leads to high equilibrium Wolbachia frequencies, it does not aid Wolbachia spread from low frequencies. Indeed, the fitness advantages that produce initial Wolbachia spread and maintain non‐CI Wolbachia remain elusive. w Mau Wolbachia infecting Drosophila mauritiana do not cause CI, despite being very similar to CI‐causing w No from Drosophila simulans (0.068% sequence divergence over 682,494 bp), suggesting recent CI loss. Using draft w Mau genomes, we identify a deletion in a CI‐associated gene, consistent with theory predicting that selection within host lineages does not act to increase or maintain CI. In the laboratory, w Mau shows near‐perfect maternal transmission; but we find no significant effect on host fecundity, in contrast to published data. Intermediate w Mau frequencies on the island of Mauritius are consistent with a balance between unidentified small, positive fitness effects and imperfect maternal transmission. Our phylogenomic analyses suggest that group‐B Wolbachia , including w Mau and w Pip, diverged from group‐A Wolbachia , such as w Mel and w Ri, 6–46 million years ago, more recently than previously estimated.