Hosts can rapidly evolve resistance in response to parasite outbreaks, yet remain susceptible to infection in the long term. We studied the impact of intermittent sexual reproduction on variation in resistance using the ecologically important zooplankton Daphnia dentifera and its virulent fungal parasite Metschnikowia bicuspidata. Hosts reproduce asexually from spring to fall but switch to sexual reproduction in early winter, creating diapausing eggs that are incorporated into lake sediments. Fungal outbreaks impose rapid directional selection for increased resistance in Daphnia dentifera populations. However, host populations maintain substantial variation in resistance phenotypes. We hypothesized that end-of-year sexual reproduction increases phenotypic and genetic diversity in the offspring, altering resistance distributions.
To test our hypothesis, we collected mothers bearing diapausing eggs from two lakes: one with high disease prevalence and one with no disease. We hatched the eggs, then maintained clonal lines of parents and offspring in the lab. We quantified the resistance phenotype of each clone using an infection assay, then measured heritability of resistance and changes in phenotypic distributions between parent and offspring populations. We used microsatellite genotyping to see changes to genotypic distributions between parent and offspring populations.
Results/Conclusions
The two lakes in the study were sampled biweekly for Metschnikowia infected hosts from September to December 2015. Maximum prevalence measures of 0.05% and 17% were obtained for Hackberry Lake (“low disease”) and Midland Lake (“high disease”), respectively. The narrow-sense heritability of susceptibility is h2 = 0.53 for Daphnia collected from the low disease lake and h2 = 0.50 for Daphnia collected from the high disease lake, confirming resistance is heritable. Infection assays show average infection prevalence in the parent group from the low disease lake ranged from 0.106 to 0.850 (mean = 0.527, SD = 0.214) while values for their offspring ranged from 0.098 to 0.781 (mean = 0.365, SD = 0.198). The average fraction of infected hosts from the parent group from the high disease lake ranged from 0 to 0.650 (mean = 0.271, SD = 0.208) while the offspring values ranged from 0 to 0.644 (mean = 0.281, SD = 0.177). However, the skewedness of these distributions may be more biologically significant and analysis is ongoing. Genotyping data collection is underway.