Data from: No evidence for induction or selection of mutant sodium channel expression in the copepod Acartia husdsonica challenged with the toxic dinoflagellate Alexandrium fundyense

Some species in the dinoflagellate genus Alexandrium spp. produce a suite of neurotoxins that block sodium channels, known as paralytic shellfish toxins (PST), which have deleterious effects on grazers. Populations of the ubiquitous copepod grazer Acartia hudsonica that have co-occurred with toxic Alexandrium spp. are better adapted than naïve populations. The mechanism of adaptation is currently unknown. We hypothesized that a mutation in the sodium channel could account for the grazer adaptation. We tested two hypotheses: (1) Expression of the mutant sodium channel could be induced by exposure to toxic Alexandrium fundyense; (2) in the absence of induction, selection exerted by toxic A. fundyense would favor copepods that predominantly express the mutant isoform. In the copepod A. hudsonica, both isoforms are expressed in all individuals in varying proportions. Thus, in addition to comparing expression ratios of wild-type to mutant isoforms for individual copepods, we also partitioned copepods into three groups: those that predominantly express the mutant (PMI) isoform, the wild-type (PWI) isoform, or both isoforms approximately equally (EI). There were no differences in isoform expression between individuals that were fed toxic and nontoxic food after three and 6 days; induction of mutant isoform expression did not occur. Furthermore, the hypothesis that mutant isoform expression responds to toxic food was also rejected. That is, no consistent evidence showed that the wild-type to mutant isoform ratios decreased, or that the relative proportion of PMI individuals increased, due to the consumption of toxic food over four generations. However, in the selected line that was continuously exposed to toxic food sources, egg production rate increased, which suggested that adaptation occurred but was unrelated to sodium channel isoform expression.

甲藻门亚历山大藻属（Alexandrium spp.）的部分物种可产生一系列阻断钠通道的神经毒素，即麻痹性贝毒（paralytic shellfish toxins, PST），该类毒素对牧食者具有毒害作用。与有毒亚历山大藻共存过的广布桡足类牧食者赫氏纺锤水蚤（Acartia hudsonica）种群，其适应能力要优于未接触过该有毒藻类的种群。目前该适应的分子机制尚不明确，本研究推测钠通道突变可解释该牧食者的适应性演化。本研究验证了两项假说：① 暴露于有毒的芬地亚历山大藻（Alexandrium fundyense）可诱导突变型钠通道的表达；② 若无诱导作用存在，有毒芬地亚历山大藻施加的选择压力将更倾向于保留主要表达突变型同工型的桡足类个体。对于赫氏纺锤水蚤而言，所有个体均会表达这两种同工型，且二者的表达比例存在个体差异。因此，本研究除了比较单个桡足类个体的野生型与突变型同工型表达比例外，还将受试桡足类划分为三组：主要表达突变型同工型（PMI）组、主要表达野生型同工型（PWI）组，以及两种同工型表达量大致相当（EI）组。分别在投喂有毒饵料与无毒饵料的个体中，于第3天和第6天检测同工型表达情况，未发现显著差异，即未观察到突变型同工型表达的诱导现象。此外，「突变型同工型表达会响应有毒饵料」这一假说同样被推翻。也就是说，历经4代投喂有毒饵料后，并未发现一致的证据表明野生型与突变型同工型的表达比例出现下降，也未发现主要表达突变型同工型的个体相对占比有所提升。但在持续暴露于有毒饵料的选育种群中，个体的产卵率出现显著提升，这表明适应性演化确实发生，但该过程与钠通道同工型的表达并无关联。