Data from: Toxin-resistant isoforms of Na+/K+-ATPase in snakes do not closely track dietary specialization on toads

Toads are chemically defended by bufadienolides, a class of cardiotonic steroids that exert toxic effects by binding to and disabling the Na+/K+-ATPases of cell membranes. Some predators, including a number of snakes, have evolved resistance to the toxic effects of bufadienolides and prey regularly on toads. Resistance in snakes to the acute effects of these toxins is conferred by at least two amino acid substitutions in the cardiotonic steroid binding pocket of the Na+/K+-ATPase. We surveyed 100 species of snakes from a broad phylogenetic range for the presence or absence of resistance-conferring mutations. We found that such mutations occur in a much wider range of taxa than previously believed. Although all sequenced species known to consume toads exhibited the resistance mutations, many of the species possessing the mutations do not feed on toads, much less specialize on that food source. This suggests that either there is little performance cost associated with these mutations or they provide an unknown benefit. Furthermore, the distribution of the mutation among major clades of advanced snakes suggests that the origin of the mutation reflects evolutionary retention more than dietary constraint.

蟾蜍依靠蟾毒配基类（bufadienolides）进行化学防御，这类强心甾类化合物可通过结合并阻断细胞膜上的钠钾ATP酶（Na+/K+-ATPase）发挥毒性作用。包括多种蛇类在内的部分捕食者已演化出对该蟾毒配基类毒素的抗性，并可常规捕食蟾蜍。蛇类对这类毒素急性毒性的抗性，由钠钾ATP酶的强心甾结合口袋中至少两个氨基酸替换所赋予。我们对涵盖广泛系统发育范围的100个蛇类物种开展了调查，以检测是否存在上述赋予抗性的突变。研究发现，这类抗性突变在演化类群中的分布范围远较此前认知更广。尽管所有已知会捕食蟾蜍的已测序蛇类物种均携带该抗性突变，但许多携带该突变的物种并不以蟾蜍为食，更不会特化依赖这类食物来源。这提示这类突变要么几乎不存在适合度代价，要么可带来未知的益处。此外，该突变在高等蛇类主要演化支中的分布模式表明，该突变的起源更倾向于演化保留而非食性约束。