RT Journal Article
SR Electronic
T1 Loss of cytoplasmic incompatibility and minimal fecundity effects explain relatively low <em>Wolbachia</em> frequencies in <em>Drosophila mauritiana</em>
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 461574
DO 10.1101/461574
A1 Megan K. Meany
A1 William R. Conner
A1 Sophia V. Richter
A1 Jessica A. Bailey
A1 Michael Turelli
A1 Brandon S. Cooper
YR 2018
UL http://biorxiv.org/content/early/2018/11/03/461574.abstract
AB Maternally transmitted Wolbachia bacteria infect about half of all insect species. Many Wolbachia cause cytoplasmic incompatibility (CI), reduced egg hatch when uninfected females mate with infected males. CI produces a frequency-dependent fitness advantage that leads to high equilibrium Wolbachia frequencies but does not aid Wolbachia spread from low frequencies. The fitness advantages that produce initial Wolbachia spread and maintain non-CI Wolbachia remain elusive. Wolbachia variant wMau that infects Drosophila mauritiana does not cause CI, despite being very closely related to the CI-causing Wolbachia wNo in D. simulans (0.068% sequence divergence over 682,494 bp), suggesting that CI was recently lost. Using draft Wolbachia genomes, we identify a deletion in a WO phage gene that may disrupt CI. We find no evidence that wMau increases host fecundity. We report intermediate and apparently stable wMau infection frequencies on the Indian Ocean island of Mauritius, consistent with no CI and no appreciable positive effect on fecundity. Our data indicate that wMau frequencies reflect a balance between unknown, weak positive effects on fitness and imperfect maternal transmission. Phylogenomic analyses suggest that Supergroup B Wolbachia, including wMau, diverged from Supergroup A Wolbachia, including wMel from D. melanogaster, 6–46 million years ago, later than previously estimated.