Collaborative Research: Costs and Advantages of a Novel Sodium Channel Mutation in Copepods

有毒藻华对渔业和公共卫生构成威胁。了解有毒藻类对水生生态系统影响的一个关键问题是食草动物如何进化适应藻类毒素。桡足类（海洋中最丰富的多细胞动物）对产生强效神经毒素（称为石房蛤毒素，STX）的微藻的适应性先前已经得到证实。STX阻断钠（Na+）通道并中断神经传递信号。一种位于Na+通道内部的新突变，当通道失活时（即，泄漏信道）。泄漏通道导致非预期的神经传递信号和细胞超敏反应;因此，它们被认为对个体来说非常昂贵。然而，假设在STX存在下，漏通道突变是有利的，因为漏通道的STX阻断降低了非预期神经传递信号和细胞超敏反应的可能性。该项目代表了康涅狄格大学和佛罗里达大学实验室在分子技术、神经生物学和浮游动物生态学和进化方面的跨学科合作。预期成果如下：1）开发用于特异性检测个体桡足类中的野生型和突变型Na+通道的遗传标记，2）突变型Na+通道的功能特性及其对STX的响应的神经生理学表征，3）量化携带导致渗漏Na+通道的突变的个体的成本和益处。这项研究可能会证明神经毒素适应的新分子机制，并为从神经生物学到生态学和进化的各个研究领域提供信息。 这项研究的更广泛的影响是：1）预测食草动物是否可以控制有毒水华和毒素转移到鱼类和贝类的新的关键信息。2)与专业教育工作者合作，将这项研究的结果和毒素适应文献转化为符合国家科学标准的课程材料。这些材料将通过一个网站和在科学家和中等教育工作者会议上举办的讲习班广泛提供。3)针对外行听众的系列讲座中的介绍。4)在跨学科环境中培养本科生和研究生。

Toxic algal blooms pose a threat to fisheries and public health. A key issue for understanding the effects of toxic algae on aquatic ecosystems is how grazers evolve adaptations to algal toxins. Adaptation of copepods (the most abundant multicellular animals in the sea) to microalgae that produce potent neurotoxins (called saxitoxins, STX) has been previously demonstrated. STX blocks sodium (Na+) channels and interrupts nerve transmission signals. A novel mutation that is located in the inner portion of the Na+ channel, and leads to persistent electrical currents when the channel is inactivated (i.e., a leaky channel), has been identified. Leaky channels result in unintended nerve transmission signals and cell hypersensitivity; hence, they are considered to be very costly to individuals. However, it is hypothesized that in the presence of STX, the leaky channel mutation is advantageous because STX blockage of leaky channels reduces the likelihood of unintended nerve transmission signals and cell hypersensitivity. This project represents an interdisciplinary collaboration between labs at University of Connecticut and the University of Florida with expertise in molecular techniques, neurobiology, and zooplankton ecology and evolution. Expected results are: 1) Development of genetic markers for specifically detecting wild and mutant Na+ channels in individual copepods, 2) Neurophysiological characterization of the functional properties of the mutant Na+ channel and its responses to STX, 3) Quantification of the costs and benefits to individuals bearing the mutation responsible for the leaky Na+ channel. This research can potentially lead to the demonstration of a new molecular mechanism of neurotoxin adaptation, and inform a variety of fields of research from neurobiology to ecology and evolution. The broader impacts of this research are: 1) New key information for predicting whether grazers can control toxic blooms and toxin transfer to fish and shellfish. 2) Collaboration with professional educators to translate results from this study and the toxin adaptation literature into prepared curricular materials that meet national science standards. The material will be made widely available via a website and workshops presented at conference meetings of scientists and secondary educators. 3) Presentations in lecture series aimed at lay audiences. 4) Training of undergraduate and graduate students in an interdisciplinary environment.