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Additional file 2: Fig. S1. Percent water content of fish from different origins during the sea pen experiments. Data derived from fish of mixed (4th) sentinel pen over the course of the experiment. Significance was determined by pairwise t-testing against fish from farmed origin. F = Farmed, HFF = Hybrid Farmed Female, HWF = Hybrid Wild Female, W = Wild, Significance codes: ***p < 0.001; **p < 0.01. Fig. S2. Stacked bar plot showing the mean relative abundance of gut microbiota on phylum level for recently fed fish, starved fish (48 h feed withdrawal) and environmental control samples (feed and marine water (MW)).

Additional file 1: Table S1. Overview of the metabolic rate experiment. Sample_Id refers to individual fish. Sampling day refers to the day when fish were caught. Processing day refers to the day fish were dissected. Experiment day equals processing days, only in another format. Temperature refers to the water temperature at the sea pens on each sampling day. Table S2. First round PCR primers used for NGS library preparation. Table S3. Second round PCR primers used for NGS library preparation. Table S4. Mean length, weight and Fulton’s condition factor per genetic origin for 3 points in time (pre sea pen hatchery, date of sea pen transfer and at the termination point of the experiment). Table S5. ANCOVA results of the effect of AGD severity Score on weight adjusted SMR (left), MMR (middle) and AS (right) measures. Significance codes: *** < 0.001; ** < 0.01; * < 0.05. Table S6. Multiple comparisons of means of metabolic rate measures between different AGD severity scores (Tukey post-hoc for weight-adjusted model). Significance codes: ** < 0.01; * < 0.05. Table S7. Permanova results showing differences between gut microbial community compositions of starved and fed fish for two different timepoints T0 and T1 in PC samples. Significance codes: ** < 0.01; * < 0.05. Table S8. Permanova results showing differences between gut microbial community compositions of starved and fed fish for two different timepoints T0 and T1 in MG samples. Significance codes: ** < 0.01; * < 0.05. Table S9. Linear model for Chao1 richness estimates in MG samples calculated by the interaction term of AGD severity score and genetic origin. AGD severity of 0 and farmed origin served as baseline for comparisons. Significance codes: *** < 0.001; ** < 0.01; * < 0.05. Table S10. Permutational analysis of variance (PERMANOVA) results testing the effect of AGD severity score, genetic origin and processing day (day of gut dissection) on pyloric caeca (PC) microbial community composition based on weighted unifrac distance matrices. Table S11. Permanova of pairwise comparisons of PC samples grouped by day of their processing. Distance matrix calculated by weighted UniFrac measure. Permutations used: 9999. Significance codes: *** < 0.001; ** < 0.01; * < 0.05. Table S12. Permutational analysis of variance (PERMANOVA) results testing the effect of AGD severity score, genetic origin and processing day (day of gut dissection) on midgut (MG) microbial community composition based on weighted unifrac distance matrices. Table S13. Permutational analysis of variance (PERMANOVA) testing pairwise comparisons for midgut (MG) samples from different AGD severity groups. Distance matrix calculated by weighted UniFrac measure. Permutations used: 9999. Significance codes: **p < 0.01; *p < 0.05.

Parasites represent one of the most notable ecological forces acting in both natural and sexual selection. Their detrimental effects on host condition and reproductive success can have strong consequences on ecological and evolutionary dynamics. Particularly, host-parasite coevolution can lead to local adaptation which in turn can drive the evolution of reproductive barriers between populations and fuel speciation. As hosts are engaged in an arms race against ever-changing parasites, they rely on effective and consistent ways to transmit defenses to their progeny. The work of my thesis examines these two aspects from the host perspective. In my first two chapters I focused on the evolution of reproductive barriers in incipient ecological speciation in the three-spined stickleback (Gasterosteus aculeatus). I particularly examined the role of ecology and parasites in limiting gene flow and maintaining differentiation between lake and river stickleback populations. Following previous work in this system showing local adaptation and assortative mating preferences based on differences at the Major Histocompatibility Complex (MHC), I investigated further mechanisms of reproductive isolation: First, I tested if post-copulatory pre-zygotic reproductive barriers (e.g. gametic isolation) occurred during incipient ecological speciation between lakes and rivers. Using replicated populations and in vitro fertilization assays in a full-factorial design, I could demonstrate ecotype-specific differences in sperm concentration and velocity. Even though these differences did not translate into ecotypic gamete preference, the results suggest an increased developmental failure of the eggs fertilized by heterospecific males. This implies that genetic incompatibilities may arise early on during ecological speciation. In my second chapter I examined the role of immune local adaptation to parasites in selection against maladapted migrants. Using a field transplant experiment with wild-caught juvenile sticklebacks, I found strong costs of migration between habitats in terms of survival and condition. I could also show that differences in parasites between lake and river were linked to maladapted responses on the innate and the adaptive immune. Furthermore, evidence for habitat-specific associations between local parasite species and locally selected MHC alleles provided insight into the maintenance of MHC diversity at the metapopulation level. In my final chapter I examined another aspect of the role of parasites, namely the role of paternal non-genetic effects of infection on life-history traits, resistance and tolerance. Until recently, non-genetic transgenerational effects mostly focused on mothers, whereas this experiment demonstrated that infected fathers could also contribute to variation in offspring phenotype. I showed paternal effects of experimental parasite infection mediated through sperm deficiency. By testing and revealing costs and benefits associated with paternal infection and controlling for genetic factors, I provided evidence for the adaptive value of non-genetic transgenerational effects of infection. Furthermore, I showed that resistance and tolerance to parasites can be shaped by both genetic and non-genetic effects. I discuss that the existence of non-genetic effects increasing offspring tolerance but not resistance can have strong consequences on host-parasite dynamics at ecological and evolutionary scales. This thesis reveals the role of parasites in promoting and maintaining diversity in their hosts, from the level of the sperm phenotype to the species level. While gametic isolation plays a minor role in ongoing ecological speciation, local adaptation to different parasite communities leads to high costs of migration. My work additionally reveals that parasites can affect phenotypic variation not only within but also across generations.