Suppression of Wolbachia mediated Cytoplasmic Incompatibility

Abstract

Insect biocontrol applications often hinge upon insect reproduction. Wolbachia are maternally inherited intracellular bacteria that infect insects. Wolbachia sterilizes a mosquito sperm resulting in a lethal embryonic phenotype called cytoplasmic incompatibility (CI), wherein eggs from un-infected females fail to develop when fertilized from Wolbachia-infected males. Contrary to this, if males and females both are infected, embryos are viable. The molecular mechanism of CI involves Wolbachia deubiquitylating enzyme CidB and its cognate partner antidote, CidA. In CHAPTER II, the process of identifying potential molecular targets and suppressors of Wolbachia’s CidB is described. By finding alleles capable of suppressing CI, we will gain insights into the molecular pathways targeted by CidB. In toto, we propose that CidB targets Kap-α, nuclear-protein import, and P32, protamine-histone exchange to induce CI. The next question was whether CidB cleaves ubiquitin directly off Kap-α or P32 to induce CI. In CHAPTER III, functional mutations and genetic modifications in these two genes were explored to test the role of these two genes in the suppression of CI in Drosophila. The work done here is important for two reasons, firstly, they provide hints toward pathways targeted by CI. Secondly, these genes might co-evolve as resistance factors to CI. Importantly, suppression of CI in vectors will reduce the effectiveness of global mosquito control efforts harnessing Wolbachia and CI.