Cardinium-Induced Cytoplasmic Incompatibility in Encarsia Parasitoid Wasps

Abstract

Most insects engage in symbioses with intracellular microbes that are transmitted from infected mothers to their offspring. Cardinium hertigii is a common symbiont, infecting ~10% of arthropods, including minute parasitoid wasps in the genus Encarsia. Cardinium increases the likelihood of its transmission by inducing cytoplasmic incompatibility (CI). In CI, crosses between infected male and uninfected female wasps result in early embryonic offspring mortality. Offspring of infected females survive regardless of male infection status, causing infected females to have higher fitness than uninfected females, and fueling Cardinium spread. Here, I investigated how the cEper1 Cardinium strain in E. suzannae responds to temperature stress, a common hurdle for symbiont maintenance in natural populations. I found that exposure to stressful temperatures during Encarsia male development modified the severity of Cardinium-induced CI. The severity of CI was only affected when exposure occurred during pupal development, suggesting a link between CI and the wasp pupal stage. I explored this link using fluorescent in-situ hybridization (FISH) to reveal Cardinium localization within developing wasp testes. Cardinium cells are abundant in testes and infect most sperm cells, but are removed from these cells during the final sperm maturation process, which is completed prior to adulthood. These results indicate that Cardinium modifies Encarsia sperm cells during their maturation process in the pupal stage. Finally, I explored the timing of another Cardinium-Encarsia CI system involving two unique strains of Cardinium infecting Encarsia partenopea. Using a combination of antibiotic trials and imaging Cardinium via FISH, I found that the lower density Cardinium strain, cEina3, is responsible for CI, and modifies sperm cells in the pupal stage. The cEina3 strain does not infect sperm cells and instead infects somatic tissue at the base of the testis and surrounding the seminal vesicle, the storage organ that houses mature sperm. As cEina3 causes severe CI, this suggests that the fatal CI factor may differ between the two strains, with the cEina3 factor more readily diffusing through cytoplasm and targeting mature sperm. Together this work will inform future research on identifying the elusive factors responsible for Cardinium-induced CI.