Cytoplasmic incompatibility

CI has been reported in many insect species (including amongst many others mosquitoes,[1] Drosophila fruit flies,[2][3] flour beetles,[4] snout moths[5] and parasitoid wasps[6]), as well as in mites[7] and woodlice.

Several landmark studies in the 2010s[23][24][25] paved the way to use CI-inducing Wolbachia for controlling suppressing diseases such as dengue fever in mosquitoes.

In contrast, CI in haplodiploid hosts can also manifest as embryonic mortality, but may also in some species lead to haploid offspring that then develop into males.

The closely related species of the wasp Nasonia show embryonic mortality as well as male development among incompatible crosses.

Because Wolbachia are absent from mature sperm and appear to be excluded during the individualization process, the modification must occur before the conclusion of spermatogenesis.

[30] The second event, called rescue, takes place inside the fertilized egg where Wolbachia presence prevents CI from occurring.

As long as the Wolbachia strains in egg and sperm cells correspond, harmful effects cannot be observed on a cellular level.

As a secondary consequence, stemming from this asynchrony, the paternal chromosomes do not properly condense and align on the metaphase plate during the first mitosis.

When the CI-inducing bacteria are rare in the population, there will be only few incompatible matings and selection (or drive) towards higher frequencies will only be weak.

[36] The invasion threshold may be overcome through random genetic drift and therefore facilitated by small (at least locally) population sizes.