The Essay on Cytoplasmic Incompatibility
The genetic basis of the wMel cytoplasmic incompatibility are simple CI factor genes, cifA and cifB, encoded by WO prophage regions in the wMel genome. Double transgene expression in the testes of D. melanogaster causes CI, and cifA expression alone in the ovaries rescues CI 14,48,49. Wolbachia-mediated cytoplasmic incompatibility CI is an insect sterility syndrome controlled by the protein effectors CidA and CidB. By characterizing the distribution and impact of CidA and CidB in Drosophila and Culex mosquitoes, Horard et al. showed that CidA and CidB function as a transgenerational toxin antidote system for: Male sterility MS and self-incompatibility SI 1. 1 1 Male sterility MS Lasa and Bosemark 1993 saw male sterility in plants as an inability to produce or release functional pollen and is the result of the failure of the formation or development of functional stamens, microspores or gametes. The discovery of two genes encoded by Wolbachia prophage WO that functionally recapitulate and amplify cytoplasmic incompatibility in arthropods is the first step toward solving the problem. the genetic. Wolbachia are intracellular, maternally inherited bacteria with an impressive history of adaptation to intracellular lifestyles. Rather than adapting to a single host lineage, Wolbachia evolved ways to jump across host species and establish relatively stable associations maintained by vertical transmission. Wolbachia are capable of this. For example, a classic example is the wave of Wolbachia inducing cytoplasmic incompatibility CI that swept through Californian D. simulans populations in Turelli and The most commonly observed manipulation is cytoplasmic incompatibility CI. CI leads to embryonic death in crosses b, Wolbachia are maternally inherited endosymbiotic bacteria, widespread among arthropods due to host reproductive manipulations that increase their prevalence in host populations.