Cytoplasmic incompatibility

Unidirectional CI: Mating of infected males and uninfected females results in CI. All other crosses are compatible.
Bidirectional CI: Mating of males infected with Wolbachia strain I and females infected by Wolbachia strain II (and vice versa) results in CI.

CI occurs when a Wolbachia infected male mates with a female that is infected by another Wolbachia strain (bidirectional CI) or is uninfected (unidirectional CI). Any other combination of un-/infected male/female crosses are compatible. An infected female is compatible with any uninfected male, or with any male infected with the same Wolbachia strain. On the other hand, an uninfected female is only compatible with an uninfected male. In other words, if the male is infected by a CI-inducing strain of Wolbachia that is non-existent in its mate, it is an incompatible cross.[2] Turelli et al. 2018 finds that CI can be resolved by infection of the females with the same strain that is affecting the males, which imposes a population level incentive in favour of CI-inducing strains of Wolbachia. They also find that this propagates the WO phage.[3] Hosts can be cured from Wolbachia infection by antibiotic use.

In diploid organisms CI leads to embryonic mortality. In contrast, CI in haplodiploid hosts may lead to haploid (and thus male) offspring. The closely related species of the wasp Nasonia show embryonic mortality as well as male development among incompatible crosses. In N. vitripennis, however, the vast majority of the CI embryos are converted into males.[4]

There are two distinguished events that lead to the CI inducing manipulation. The first occurs inside the Wolbachia infected male during spermatogenesis and is called modification. 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.[5] 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.

A major consequence of CI is the delayed entry into mitosis of the male pronucleus. 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. As a consequence, only the maternal chromosome segregate normally, producing haploid embryos.[6] The rescue of CI by infected eggs leads to the restoration of synchrony between the female and the male pronucleus.[6][7]

The exact mechanisms of how Wolbachia perform modification and rescue are unknown. In Drosophila, the earliest effects caused by CI can already be observed during the sperm chromatin remodeling of the paternal chromosomes.[8] However, it was also observed that in other host species, the defects caused by CI only occur much later in development [9]

CI, as described by Werren,[2] results in selection pressure on uninfected males, as infected females can mate both with uninfected males and infected males, but uninfected females cannot mate with infected males. As Wolbachia are only transmitted by females, this mechanism promotes the spread of Wolbachia and therefore keeps Wolbachia from dying out because of incomplete transmission. This has led to discoveries in control of disease transmission by using Wolbachia to control the reproduction of a population by introducing Wolbachia-infected males.[10] This has been seen in the Aedes, mosquito, family, in the Aedes albopictus and Aedes aegypti species.

Wolbachia are not the only bacteria capable of inducing CI. For example, researchers have found that infection by bacteria of the genus Cardinium can also result in CI.[13]

• Wolbachia
• Cardinium
• Endosymbiont
• Intragenomic conflict