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It is unclear whether transport by human vectors can increase the robustness of translocated populations and thereby enhance their invasiveness. To test this concept, we investigated the effect of heat stress on the tolerance of mussel populations towards a second stress event of the same kind. The heat challenges we mimicked can be faced by marine invertebrates that are transported through regions with high sea surface temperatures on ship hulls or in ballast water tanks. The study included 5 mussel species that were collected at sites in Brazil, Chile, Finland, Germany (Baltic Sea) and Portugal. In parallel laboratory experiments, monospecific groups of individuals were exposed to heat challenges that caused 60–83% mortality in the experimental groups within 15–28 days. The surviving individuals were exposed to a second stress event of the same kind, while their survival was then compared to the robustness of conspecifics that had not been exposed to elevated temperatures before. We observed that thermal tolerance was significantly enhanced by previous heat stress experience in case of Semimytilus algosus from Chile and in case of Mytilus edulis from Germany. Our results suggest that heat challenges, which marine invertebrates experience during transport, can enhance stress tolerance in founder populations of these species in their non-native range by potentially increasing the frequency of genetically adapted genotypes. This points at the necessity to learn more about selection acting on organisms during human-mediated transport—in the aquatic but also in the terrestrial environment.

It is unclear whether transport by human vectors can increase the robustness of translocated populations and thereby enhance their invasiveness. To test this concept, we investigated the effect of heat stress on the tolerance of mussel populations towards a second stress event of the same kind. The heat challenges we mimicked can be faced by marine invertebrates that are transported through regions with high sea surface temperatures on ship hulls or in ballast water tanks. The study included 5 mussel species that were collected at sites in Brazil, Chile, Finland, Germany (Baltic Sea) and Portugal. In parallel laboratory experiments, monospecific groups of individuals were exposed to heat challenges that caused 60–83% mortality in the experimental groups within 15–28 days. The surviving individuals were exposed to a second stress event of the same kind, while their survival was then compared to the robustness of conspecifics that had not been exposed to elevated temperatures before. We observed that thermal tolerance was significantly enhanced by previous heat stress experience in case of Semimytilus algosus from Chile and in case of Mytilus edulis from Germany. Our results suggest that heat challenges, which marine invertebrates experience during transport, can enhance stress tolerance in founder populations of these species in their non-native range by potentially increasing the frequency of genetically adapted genotypes. This points at the necessity to learn more about selection acting on organisms during human-mediated transport—in the aquatic but also in the terrestrial environment.

The consequences of emerging marine diseases on the evolutionary trajectories of affected host populations in the marine realm are largely unexplored. Evolution in response to natural selection depends on the genetic variation of the traits under selection and the interaction of these traits with the environment (GxE). However, in the case of diseases, genotypes of pathogens add another dimension to this interaction. Therefore, the study of disease resistance needs to be extended to the interaction of host genotype, pathogen genotype and environment (GxGxE). In the present study we used a full-sib breeding design crossing two genetically differentiated populations of the Pacific oyster Crassostrea gigas (Thunberg, 1793), to determine the influence of host genotype, pathogen genotype and temperature on disease resistance. Based on a controlled infection experiment on two early life stages, i.e. D-larvae and Pediveliger larvae at elevated and ambient water temperatures we estimated disease resistance to allopatric and sympatric Vibrio sp. by measuring survival and growth within and between genetically differentiated oyster populations. In both populations survival was higher upon infection with sympatric Vibrio sp. indicating that disease resistance has a genetic basis and is dependent on host genotype. In addition we observed a significant GxGxE effect in D-larvae, where contrary to expectations, disease resistance was higher at warm than at cold temperatures. Using thermal reaction norms, we could further show, that disease resistance is an environment dependent trait with high plasticity, which indicates the potential for a fast acclimatization to changing environmental conditions. These population specific reaction norms disappeared in hybrid crosses between both populations which demonstrates that admixture between genetically differentiated populations can influence GxGxE interactions on larger scales.

The consequences of emerging marine diseases on the evolutionary trajectories of affected host populations in the marine realm are largely unexplored. Evolution in response to natural selection depends on the genetic variation of the traits under selection and the interaction of these traits with the environment (GxE). However, in the case of diseases, genotypes of pathogens add another dimension to this interaction. Therefore, the study of disease resistance needs to be extended to the interaction of host genotype, pathogen genotype and environment (GxGxE). In the present study we used a full-sib breeding design crossing two genetically differentiated populations of the Pacific oyster Crassostrea gigas (Thunberg, 1793), to determine the influence of host genotype, pathogen genotype and temperature on disease resistance. Based on a controlled infection experiment on two early life stages, i.e. D-larvae and Pediveliger larvae at elevated and ambient water temperatures we estimated disease resistance to allopatric and sympatric Vibrio sp. by measuring survival and growth within and between genetically differentiated oyster populations. In both populations survival was higher upon infection with sympatric Vibrio sp. indicating that disease resistance has a genetic basis and is dependent on host genotype. In addition we observed a significant GxGxE effect in D-larvae, where contrary to expectations, disease resistance was higher at warm than at cold temperatures. Using thermal reaction norms, we could further show, that disease resistance is an environment dependent trait with high plasticity, which indicates the potential for a fast acclimatization to changing environmental conditions. These population specific reaction norms disappeared in hybrid crosses between both populations which demonstrates that admixture between genetically differentiated populations can influence GxGxE interactions on larger scales.

The consequences of emerging marine diseases on the evolutionary trajectories of affected host populations in the marine realm are largely unexplored. Evolution in response to natural selection depends on the genetic variation of the traits under selection and the interaction of these traits with the environment (GxE). However, in the case of diseases, genotypes of pathogens add another dimension to this interaction. Therefore, the study of disease resistance needs to be extended to the interaction of host genotype, pathogen genotype and environment (GxGxE). In the present study we used a full-sib breeding design crossing two genetically differentiated populations of the Pacific oyster Crassostrea gigas (Thunberg, 1793), to determine the influence of host genotype, pathogen genotype and temperature on disease resistance. Based on a controlled infection experiment on two early life stages, i.e. D-larvae and Pediveliger larvae at elevated and ambient water temperatures we estimated disease resistance to allopatric and sympatric Vibrio sp. by measuring survival and growth within and between genetically differentiated oyster populations. In both populations survival was higher upon infection with sympatric Vibrio sp. indicating that disease resistance has a genetic basis and is dependent on host genotype. In addition we observed a significant GxGxE effect in D-larvae, where contrary to expectations, disease resistance was higher at warm than at cold temperatures. Using thermal reaction norms, we could further show, that disease resistance is an environment dependent trait with high plasticity, which indicates the potential for a fast acclimatization to changing environmental conditions. These population specific reaction norms disappeared in hybrid crosses between both populations which demonstrates that admixture between genetically differentiated populations can influence GxGxE interactions on larger scales.