Wolbachia are a group of bacteria that infect a major proportion of insect species. They are known for intricate manipulations of their host’s reproduction. The most puzzling manipulation is called Cytoplasmic Incompatibility (CI). In males, CI consists of Wolbachia manipulating the sperm in a yet unknown way – this manipulation is called mod (for modification). DNA from modified sperm cannot properly participate in the first embryonic mitosis, except if Wolbachia action in the egg recovers the functionality of the sperm DNA.
Owing to the nature of CI, a female can only successfully mate with an infected male if she is herself infected by an appropriate Wolbachia strain. If such an infected female mates with an uninfected male, there are no defects. Therefore, infected females have a selective advantage over uninfected ones, helping Wolbachia spread. Considering that CI effectively inhibits certain crosses, Wolbachia infection could lead to reproductive isolation or gene flow reduction between host populations with different infection statuses. Therefore, CI in Wolbachia may play an important role in insect speciation. A deeper insight into the mechanism behind Wolbachia-induced CI is likely to further our understanding of host evolutionary dynamics.
A New Model and Method for Understanding Wolbachia-Induced Cytoplasmic Incompatibility. 2011 PLoS ONE 6(5): e19757. doi:10.1371/journal.pone.0019757
Wolbachia are intracellular bacteria transmitted almost exclusively vertically through eggs. In response to this mode of transmission, Wolbachia strategically manipulate their insect hosts’ reproduction. In the most common manipulation type, cytoplasmic incompatibility, infected males can only mate with infected females, but infected females can mate with all males. The mechanism of cytoplasmic incompatibility is unknown; theoretical and empirical findings need to converge to broaden our understanding of this phenomenon. For this purpose, two prominent models have been proposed: the mistiming-model and the lock-key-model. The former states that Wolbachia manipulate sperm of infected males to induce a fatal delay of the male pronucleus during the first embryonic division, but that the bacteria can compensate the delay by slowing down mitosis in fertilized eggs. The latter states that Wolbachia deposit damaging “locks” on sperm DNA of infected males, but can also provide matching “keys” in infected eggs to undo the damage. The lock-key-model, however, needs to assume a large number of locks and keys to explain all existing incompatibility patterns. The mistiming-model requires fewer assumptions but has been contradicted by empirical results. We therefore expand the mistiming-model by one quantitative dimension to create the new, so-called goalkeeper-model. Using a method based on formal logic, we show that both lock-key- and goalkeeper-model are consistent with existing data. Compared to the lock-key-model, however, the goalkeeper-model assumes only two factors and provides an idea of the evolutionary emergence of cytoplasmic incompatibility. Available cytological evidence suggests that the hypothesized second factor of the goalkeeper-model may indeed exist. Finally, we suggest empirical tests that would allow to distinguish between the models. Generalizing our results might prove interesting for the study of the mechanism and evolution of other host-parasite interactions.