Wolbachia cifB induces cytoplasmic incompatibility in the malaria mosquito vector

Wolbachia, a maternally inherited intracellular bacterial species, can manipulate host insect reproduction by cytoplasmic incompatibility (CI), which results in embryo lethality in crosses between infected males and uninfected females. CI is encoded by two prophage genes, cifA and cifB. Wolbachia, coupled with the sterile insect technique, has been used in field trials to control populations of the dengue vector Aedes albopictus, but CI-inducing strains are not known to infect the malaria vector Anopheles gambiae. Here we show that cifA and cifB can induce conditional sterility in the malaria vector An. gambiae. We used transgenic expression of these Wolbachia-derived genes in the An. gambiae germline to show that cifB is sufficient to cause embryonic lethality and that cifB-induced sterility is rescued by cifA expression in females. When we co-expressed cifA and cifB in male mosquitoes, the CI phenotype was attenuated. In female mosquitoes, cifB impaired fertility, which was overcome by co-expression of cifA. Our findings pave the way towards using CI to control malaria mosquito vectors. Wolbachia cifB expression in Anopheles gambiae males is sufficient to induce cytoplasmic incompatibility that is sensitive to the expression level of the factors involved.

Automated summary

Two prophage genes, cifA and cifB from Wolbachia, are found to induce conditional sterility in the malaria vector Anopheles gambiae. The expression of cifB in An. gambiae males is sufficient to cause cytoplasmic incompatibility, which is sensitive to the expression levels of the factors involved. Co-expression of cifA can rescue the fertility impairment caused by cifB in female mosquitoes. These findings pave the way for potential use of cytoplasmic incompatibility to control malaria mosquito vectors.