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 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.

蟾蜍通过蟾毒配基类（bufadienolides）进行化学防御：这类强心甾类化合物（cardiotonic steroids）可通过结合并抑制细胞膜上的钠钾ATP酶（Na+/K+-ATPase）发挥毒性作用。部分捕食者（包括多种蛇类）已演化出对该类毒素毒性的抗性，并常规以蟾蜍为食。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。本研究针对覆盖广泛系统发育谱系的100种蛇类，开展了抗性赋予突变存在性的筛查。研究发现，这类突变在类群中的分布范围远较此前认知更广。尽管所有已知以蟾蜍为食的蛇类均携带该抗性突变，但诸多携带该突变的蛇类并不以蟾蜍为食，更不会特化依赖此类食物资源。这表明，要么这类突变几乎不会带来适合度代价，要么它们具备尚未被发现的益处。此外，高等蛇类主要演化支中该突变的分布模式提示，该突变的起源更多反映了演化保留效应，而非食性约束的影响。