Author:
Fletcher Jessica,Malhotra Anita,Wüster Wolfgang
Abstract
Predators exploiting chemically defended prey are generally resistant to prey toxins. However, toxin resistance usually incurs a fitness cost and is therefore often lost when no longer needed. Bufonid toads are a frequently abundant food resource, but chemically defended by a group of cardiotonic steroids, bufadienolides. Bufophagous predators have evolved a specific and near-universal mechanism of resistance to these toxins, consisting of two amino acid substitutions in the Na+/K+-ATPase H1–H2 extracellular domain. The dynamics of loss or retention of this adaptation in secondarily non-bufophagous lineages remain inadequately understood. Here we explore this topic by showing that the piscivorous banded water cobra Naja annulata retains the bufadienolide-resistant genotype of the otherwise toad-eating cobra clade. This confirms a trend for secondarily non-toad-eating snakes to retain bufadienolide resistance. Keywords: Antipredator adaptation, cardiotonic steroid, cardiac glycoside, evolution, piscivory
Publisher
British Herpetological Society
Cited by
1 articles.
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