One prophage WO gene rescues cytoplasmic incompatibility in <i>Drosophila melanogaster</i>.

Abstract

<i>Wolbachia</i> are maternally inherited, intracellular bacteria at the forefront of vector control efforts to curb arbovirus transmission. In international field trials, the cytoplasmic incompatibility (CI) drive system of <i>w</i>Mel <i>Wolbachia</i> is deployed to replace target vector populations, whereby a <i>Wolbachia</i>-induced modification of the sperm genome kills embryos. However, <i>Wolbachia</i> in the embryo rescue the sperm genome impairment, and therefore CI results in a strong fitness advantage for infected females that transmit the bacteria to offspring. The two genes responsible for the <i>w</i>Mel-induced sperm modification of CI, <i>cifA</i> and <i>cifB</i>, were recently identified in the eukaryotic association module of prophage WO, but the genetic basis of rescue is unresolved. Here we use transgenic and cytological approaches to demonstrate that maternal <i>cifA</i> expression independently rescues CI and nullifies embryonic death caused by <i>w</i>Mel <i>Wolbachia</i> in <i>Drosophila melanogaster</i> Discovery of <i>cifA</i> as the rescue gene and previously one of two CI induction genes establishes a "Two-by-One" model that underpins the genetic basis of CI. Results highlight the central role of prophage WO in shaping <i>Wolbachia</i> phenotypes that are significant to arthropod evolution and vector control.