Wolbachia is a bacterium that infects arthropods, such as insects and nematodes. Wolbachia has attracted a lot of attention from the researchers world-wide because it can prevent certain viruses, including Zika, dengue and chikungunya from replicating in mosquitos and transmitting them to humans. Infection with Wolbachia, however, also affects the reproduction of their insect host. The bacterium often replicates in the germline of insects. Replication in the germline allows the bacterium to be passed on to the next generation of insects and also causes a phenomenon known as cytoplasmic incompatibility (CI). CI leads to reproductive incompatibility between insects of the same species if they don’t have compatible Wolbachia infection statuses. An uninfected female fly, for example, is only able to reproduce with uninfected males because the offspring from mating with the infected males die in the early stages of development. By contrast, infected females can reproduce with both infected and uninfected males and their offspring will survive. Such incompatibility creates a selective pressure that favours infected females as they have more chances to reproduce. However, while the exact molecular mechanisms behind CI have not yet been understood, a recent study published in journal Nature shows that viral genes present in Wolbachia are partially responsible for CI.
While different Wolbachia strains can induce CI, the researches who conducted the study reasoned, that the CI-causing genes should be common between the different CI-inducing strains. Among the 161 common genes between the strains there were only two genes that were also present and expressed in the ovary cells of the flies. Interestingly, both of these genes were derived from a genome of an integrated bacterial virus, called WO. WO is also sometimes referred to as a cryptic prophage because, as far as we know, its genome, while present in the bacterial cell, is inactive and cannot make replicating viral particles. The two WO genes identified have no known functions, although, one of them has some structural similarities to protein-degrading enzymes in other viruses. Interestingly, phylogenetic analyses of these two genes, named cifA and cifB, showed that these genes are under different selection pressures than normal Wolbachia or prophage genes.
To investigate cifA and cifB are involved in CI, scientists made male flies that expressed the two genes but were not infected with the Wolbachia. The offspring from uninfected females and cifA/cifB-expressing males had 68% lower survival rate than the offspring between uninfected flies. Importantly, when cifA/cifB-expressing males mated with Wolbachia infected females all of the offspring survived, indicating that the two genes are linked to CI.
Generally, it has been observed that CI is caused by an aberrant cell division during the formation of insect embryo. Indeed, just expressing cifA and cifB genes in the flies was sufficient to reproduce the observable defects in embryo cell division. Correct embryogenesis can, however, be restored if cifA/cifB-expressing male mated with Wolbachia infected female.
This study is the first to identify molecular components of cytoplasmic incompatibility. We still do not know what exactly cifA and cifB genes do to induce CI or how their expression is regulated. Better understanding of CI may help us to explain its effects on arthropod speciation. CI is found in many arthropods and it prevents successful cross-species mating by causing the death of hybrid offspring. Further studies of CI-linked genes have important practical applications too. CI has potential uses in biological pest control methods as well as a methods for preventing infectious disease transmission by insect vectors.
LePage, Daniel P., et al. “Prophage WO genes recapitulate and enhance Wolbachia-induced cytoplasmic incompatibility.” Nature (2017).