Abstract Bacterial endosymbionts manipulate reproduction in arthropods to increase their prevalence in the host population. One such manipulation is cytoplasmic incompatibility (CI), wherein the bacteria sabotage sperm in infected males to reduce the hatch rate when mated with uninfected females, but zygotes are ‘rescued’ when that male mates with an infected female. In the spiderMermessus fradeorum(Linyphiidae),Rickettsiellasymbionts cause variable levels of CI. We hypothesised that temperature affects the strength of CI and its rescue inM. fradeorum, potentially mediated by bacterial titre. We rearedRickettsiella‐infected spiders in two temperature conditions (26°C vs. 20°C) and tested CI induction in males and rescue in females. In incompatible crosses between infected males and uninfected females, the hatch rate from warm males was doubled (mean ± standard error = 0.687 ± 0.052) relative to cool males (0.348 ± 0.046), indicating that CI induction is weaker in warm males. In rescue crosses between infected females and infected males, female rearing temperature had a marginal effect on CI rescue, but the hatch rate remained high for both warm (0.960 ± 0.023) and cool females (0.994 ± 0.004). Bacterial titre, as measured by quantitative polymerase chain reaction, was lower in warm than cool spiders, particularly in females, suggesting that bacterial titre may play a role in causing the temperature‐mediated changes in CI.
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Cardinium Localization During Its Parasitoid Wasp Host’s Development Provides Insights Into Cytoplasmic Incompatibility
Arthropods harbor heritable intracellular symbionts that may manipulate host reproduction to favor symbiont transmission. In cytoplasmic incompatibility (CI), the symbiont sabotages the reproduction of infected males such that high levels of offspring mortality result when they mate with uninfected females. In crosses with infected males and infected females, however (the “rescue” cross), normal numbers of offspring are produced. A common CI-inducing symbiont, Cardinium hertigii , causes variable levels of CI mortality in the parasitoid wasp, Encarsia suzannae. Previous work correlated CI-induced mortality with male development time in this system, although the timing of Cardinium CI-induction and the relationship between development time and CI mortality was not well understood. Here, using a combination of crosses, manipulation of development time, and fluorescence microscopy, we identify the localization and the timing of the CI-induction step in the Cardinium-E. suzannae system. Antibiotic treatment of adult Cardinium -infected males did not reduce the mortality associated with the CI phenotype, suggesting that CI-alteration occurs prior to adulthood. Our results suggest that the alteration step occurs during the pupal period, and is limited by the duration of pupal development: 1) Encarsia produces most sperm prior to adulthood, 2) FISH localization of Cardinium in testes showed an association with sperm nuclei throughout spermatogenesis but not with mature sperm, and 3) two methods of prolonging the pupal period (cool temperatures and the juvenile hormone analog methoprene) both caused greater CI mortality, suggesting the degree of alteration is limited by the duration of the pupal stage. Based on these results, we compare two models for potential mechanisms of Cardinium sperm modification in the context of what is known about analogous mechanisms of Wolbachia , a more extensively studied CI-inducing symbiont.
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- Award ID(s):
- 2002934
- PAR ID:
- 10230191
- Date Published:
- Journal Name:
- Frontiers in Microbiology
- Volume:
- 11
- ISSN:
- 1664-302X
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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