Department of Marine Sciences, University of Connecticut 1080 Shennecossett Road, Groton, Connecticut, 06340-6098.
Department of Arts and Sciences, Maine Maritime Academy 54 Pleasant Street, Castine, Maine, 04420.
Ecol Evol. 2014 Sep;4(17):3470-81. doi: 10.1002/ece3.1197. Epub 2014 Aug 22.
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.
某些甲藻属物种会产生一系列阻断钠通道的神经毒素，称为麻痹性贝类毒素（PST），这些毒素对摄食者有有害影响。与有毒的亚历山大藻属物种共同存在的无处不在的桡足类摄食者毛颚小环指猛水蚤种群比原始种群更适应。适应的机制目前尚不清楚。我们假设钠通道的突变可能是摄食者适应的原因。我们检验了两个假设：（1）暴露于有毒的亚历山大藻属芬迪湾种会诱导突变型钠通道的表达；（2）在没有诱导的情况下，有毒的 A. fundyense 选择会有利于主要表达突变型同工型的桡足类。在桡足类 A. hudsonica 中，两种同工型都在所有个体中以不同的比例表达。因此，除了比较个体桡足类的野生型到突变型同工型的表达比率外，我们还将桡足类分为三组：主要表达突变型（PMI）同工型、野生型（PWI）同工型或两种同工型大致相等（EI）的个体。在连续投喂有毒和无毒食物 3 天和 6 天后，个体之间同工型表达没有差异；未诱导突变型同工型表达。此外，突变型同工型表达响应有毒食物的假设也被拒绝。也就是说，没有一致的证据表明，由于在四代内食用有毒食物，野生型到突变型同工型的比率降低，或者 PMI 个体的相对比例增加。然而，在连续暴露于有毒食物源的选择系中，产卵率增加，这表明适应发生了，但与钠通道同工型表达无关。
