From Wolbachia genomics to phenotype: molecular models of cytoplasmic incompatibility must account for the multiplicity of compatibility types

Abstract

Wolbachia endosymbionts commonly induce cytoplasmic incompatibility, making infected males’ sperm lethal to the embryos unless these are rescued by the same bacterium, inherited from their mother. Causal genes were recently identified but two families of mechanistic models are still opposed. In the toxin–antidote model, interaction between the toxin and the antidote is required for rescuing the embryos. In host modification models, a host factor is misregulated in sperm and rescue occurs through compensation or withdrawal of this modification. While these models have been thoroughly discussed, the multiplicity of compatibility types, that is, the existence of many mutually incompatible strains, as seen in Culex mosquitoes, has not received sufficient attention. To explain such a fact, host modification models must posit that the same embryonic defects can be induced and rescued through a large variety of host targets. Conversely, the toxin–antidote model simply accommodates this pattern in a lock–key fashion, through variations in the toxin–antidote interaction sites.