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首页> 外文期刊>Journal of Experimental Marine Biology and Ecology >A novel mutation from gene splicing of a voltage-gated sodium channel in a marine copepod and its potential effect on channel function
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A novel mutation from gene splicing of a voltage-gated sodium channel in a marine copepod and its potential effect on channel function

机译：海洋co足类中电压门控钠通道基因剪接的新型突变及其对通道功能的潜在影响

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The saxitoxins (STX), a group of potent neurotoxins produced by some marine algae (dinoflagellates and cyanobacteria), block voltage-gated sodium channels, inhibiting nerve-signal transmission in consumers of STX-bearing prey. Populations of grazers (clams and copepods) persistently exposed to the STX-bearing dinoflagellate Alexandrium fundyense are less susceptible to STX than naive ones. Adaptation to STX in clams is linked to a point mutation at the STX-binding site in the sodium channel, which dramatically lowers the sensitivity to the toxin (STX resistance). The present study tested if a similar mechanism of STX resistance occurs in the copepod Acartia hudsonica. Our cloning and sequencing results indicate that two full-length cDNA variants (AhNa(v)1 and AhNa(v)2) of the sodium channel exist in A. hudsonica, which result from alternative splicing of the single coding gene. Both variants have identical nucleotide sequences except that AhNa(v)1 (the putative mutant isoform) contains a three-amino-acid (GRD) insertion and a single adjacent aa-substitution (A to V) close to the inactivation gate on the cytoplasmic linker between domains III and IV of the sodium channel. All individuals express both AhNa(v)1 and AhNa(v)2 in varying proportions. The functional consequences of the mutation were studied by inserting the three-amino acid codons into a rat (rNa(v)31.2) sodium channel expressed in both Xenopus oocytes and HEK cells. Currents carried by construct rNa(v)1.2 bearing the GRD insertion did not inactivate as completely, and recovered faster from inactivation than rNa(v)1.2. These two rNa(v)1.2 constructs were, however, equally sensitive to STX, suggesting that the GRD variation does not confer STX resistance on the rat sequence of Na(v)1.2. These results render unlikely the hypothesis that this novel mutation is responsible for the adaptation (via resistance) of A. hudsonica to STX-bearing prey. (C) 2015 Elsevier B.V. All rights reserved.
机译：毒素（STX）是由某些海藻（鞭毛藻和蓝细菌）产生的一组有效的神经毒素，可阻断钠离子通道的电压门控，从而抑制了携带STX的猎物消费者的神经信号传递。持续暴露于带有STX的甲鞭毛亚历山大鞭毛虫的放牧者（蛙类和co足类）种群比幼稚的种群对STX的敏感性较低。蛤类对STX的适应性与钠通道中STX结合位点的点突变有关，这大大降低了对毒素的敏感性（STX抗性）。本研究测试了在pe足类A螨中是否存在类似的STX抗性机制。我们的克隆和测序结果表明，A。hudsonica存在钠通道的两个全长cDNA变体（AhNa（v）1和AhNa（v）2），这是由单个编码基因的可变剪接造成的。除了AhNa（v）1（推定的突变体同工型）包含一个三氨基酸（GRD）插入物和靠近细胞质上失活门的单个相邻aa取代基（A到V），两个变体具有相同的核苷酸序列钠通道的结构域III和IV之间的连接子。所有个体均以不同比例表达AhNa（v）1和AhNa（v）2。通过将三氨基酸密码子插入在非洲爪蟾卵母细胞和HEK细胞中表达的大鼠（rNa（v）31.2）钠通道中，研究了突变的功能后果。带有GRD插入的构建体rNa（v）1.2携带的电流并未完全失活，并且从失活中恢复的速度比rNa（v）1.2快。但是，这两个rNa（v）1.2构建体对STX同样敏感，这表明GRD变异不会赋予Na（v）1.2大鼠序列以STX抗性。这些结果不太可能得出这样的假说，即该新突变是导致介壳线虫对带有STX的猎物的适应（通过抗性）的原因。 （C）2015 Elsevier B.V.保留所有权利。

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