Parental effects on tolerance to environmental stress in river-dwelling salmonids of Switzerland

Anthropogenic changes in the environment are a major force acting upon natural populations. A better understanding of the genetic and environmental components of stress tolerance is fundamental in predicting the ability of populations to cope with environmental changes. Salmonids are excellent model species for studying the components of stress tolerance because the parental effects on offspring phenotypes can be conveniently disentangled in experimental breeding crosses and are informative proxies for different components of phenotypic variance. The sire effect is a proxy for additive genetic effects, the dam effect is a proxy for the combination of additive genetic and maternal environmental effects, and the interaction effect between sire and dam is a proxy for non-additive genetic effects. In this thesis, we studied parental effects in river-dwelling salmonids of Switzerland, the brown trout (Salmo trutta) and the European grayling (Thymallus thymallus), to widen our understanding of the environmental and genetic components of stress tolerance. We built up on previous studies on parental effects in salmonids by investigating specific environmental and genetic attributes of parental effects for stress tolerance, namely egg carotenoids and multilocus heterozygosity. Egg carotenoid content, a largely maternal environmental effect, was positively linked to early offspring performance and to reduced susceptibility to pathogen infection. However, embryonic consumption of carotenoids during immune defense seemed to be dependent on the stress type. Multilocus heterozygosity, a product of the interaction between the genotypes of sires and dams, was positively linked to various early life-history traits under benign conditions. Environmental stressors influenced these correlations differently. As predicted by theory, pathogen infection revealed genetic variation that was cryptic under benign conditions and increased these correlations for some phenotypes. However, an exposure to a micropollutant, the synthetic estrogen 17α-ethinylestradiol (EE2, the active compound of most oral contraceptive pills), did not significantly change the links between heterozygosity and early life-history traits. We further focused on sire effects to address questions in conservation biology. We found that different natural brown trout populations were detrimentally affected by a low concentration of EE2. Despite displaying high levels of within-population genetic diversity, such populations did not display significant additive genetic variation for tolerance to this ecologically-relevant pollutant, i.e. they did not show the potential to evolve in response to this stressor. We then studied a grayling captive breeding stock (based on F1s of a declining population) that is currently in use for population supplementation. Breeders from this captive breeding stock displayed much lower genetic diversity than their wild counterparts. Moreover, they did not display significant additive genetic variance for tolerance to EE2, which could be a consequence of their overall lack of genetic diversity. Such lack of additive genetic variation may therefore be extended to other environmental stressors. Finally, we found that captive sires produced offspring of lower viability relative to sires of the wild population. Even though individuals from this broodstock have been kept in captivity for only one generation, this could be a result of a relaxation of natural selection in the captive environment. The studied captive breeding stock may therefore not be able to effectively support its natural population. Overall, in this thesis we described various aspects of parental effects for offspring stress tolerance in different contexts. As expected, we found that sire effects, dam effects, and their interaction influenced offspring early stress tolerance. We demonstrated that such influences are complex and widely vary across stress types and phenotypes