Data from: Additive genetic variation for tolerance to estrogen pollution in natural populations of Alpine whitefish (Coregonus sp., Salmonidae)

The evolutionary potential of natural populations to adapt to anthropogenic threats critically depends on whether there exists additive genetic variation for tolerance to the threat. A major problem for water-dwelling organisms is chemical pollution, and among the most common pollutants is 17α-ethinylestradiol (EE2), the synthetic estrogen that is used in oral contraceptives and that can affect fish at various developmental stages, including embryogenesis. We tested whether there is variation in the tolerance to EE2 within Alpine whitefish. We sampled spawners from two species of different lakes, bred them in vitro in a full-factorial design each, and studied growth and mortality of embryos. Exposure to EE2 turned out to be toxic in all concentrations we tested (≥1 ng/L). It reduced embryo viability and slowed down embryogenesis. We found significant additive genetic variation in EE2-induced mortality in both species, that is, genotypes differed in their tolerance to estrogen pollution. We also found maternal effects on embryo development to be influenced by EE2, that is, some maternal sib groups were more susceptible to EE2 than others. In conclusion, the toxic effects of EE2 were strong, but both species demonstrated the kind of additive genetic variation that is necessary for an evolutionary response to this type of pollution.

自然种群适应人为威胁的进化潜力，关键取决于其是否存在针对该威胁的耐受性加性遗传变异（additive genetic variation）。水生生物面临的主要威胁之一为化学污染，其中最常见的污染物之一是17α-乙炔雌二醇（17α-ethinylestradiol, EE2）——这种合成雌激素常用于口服避孕药，可在多个发育阶段对鱼类造成影响，包括胚胎发育（embryogenesis）。本研究以高山白鲑（Alpine whitefish）为研究对象，检测其种群内对EE2的耐受性是否存在差异。我们从两个不同湖泊的两个白鲑物种中采集产卵亲鱼，分别采用全因子实验设计（full-factorial design）进行体外繁育，并观察胚胎的生长与死亡情况。实验结果显示，在我们测试的所有浓度（≥1 ng/L）下，EE2暴露均具有毒性：它会降低胚胎存活率（embryo viability），并延缓胚胎发育进程。我们在两个物种中均发现，EE2诱导的死亡率存在显著的加性遗传变异，即不同基因型对雌激素污染的耐受性存在差异。此外，我们还发现胚胎发育的母体效应（maternal effects）会受到EE2的影响：部分母系同胞群对EE2的敏感性显著高于其他同胞群。综上，EE2的毒性效应十分显著，但两个物种均存在针对此类污染产生进化响应所需的加性遗传变异。