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<p>As an invasive species in northern Australia, the cane toad (<i>Rhinella marina</i>) has caused the decline of many native predator populations that lack resistance to toad toxin. Freshwater crocodiles (<i>Crocodylus johnstoni</i>) are particularly affected due to ingestion of cane toads, whereas saltwater crocodiles (<i>Crocodylus porosus</i>) appear to be resistant. We hypothesised that this difference in resistance may be due to sequence differences in the extracellular H1-H2 domain of the alpha subunit of the Na/K ATPase transmembrane pump, which have previously been shown to correlate with susceptibility to bufadienolides – a major component of toad toxin. Unexpectedly, predicted H1-H2 domain sequences were identical between <i>C. johnstoni</i> and <i>C. porosus</i> in all three of the candidate paralogous genes (<i>ATP1A1</i>, <i>ATP1A2</i> and <i>ATP1A3</i>) implicated in bufadienolide resistance. Moreover, sequence motifs in <i>ATP1A1</i> and <i>ATP1A3</i> were predictive of bufadienolide resistance, suggesting that other mechanisms drive cane toad toxin susceptibility in <i>C. johnstoni</i>. We discuss alternative possible explanations for our observations based on crocodilian evolution, physiology, and other active components of toad toxin.</p>

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Genetic signatures of bufadienolide resistance are poor predictors of cane toad toxin resistance in crocodilians

  • 期刊论文

  • 发表日期：

    2026年1月5日

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  • Alexandra K. Ross,
  • Pierre Ibri,
  • Jonathan K. Webb,
  • Tim S. Jessop,
  • Tim Dempster,
  • Charlotte H. Mills,
  • Tahneal Hawke,
  • Mike Letnic,
  • Stephen Frankenberg

摘要

As an invasive species in northern Australia, the cane toad (Rhinella marina) has caused the decline of many native predator populations that lack resistance to toad toxin. Freshwater crocodiles (Crocodylus johnstoni) are particularly affected due to ingestion of cane toads, whereas saltwater crocodiles (Crocodylus porosus) appear to be resistant. We hypothesised that this difference in resistance may be due to sequence differences in the extracellular H1-H2 domain of the alpha subunit of the Na/K ATPase transmembrane pump, which have previously been shown to correlate with susceptibility to bufadienolides – a major component of toad toxin. Unexpectedly, predicted H1-H2 domain sequences were identical between C. johnstoni and C. porosus in all three of the candidate paralogous genes (ATP1A1, ATP1A2 and ATP1A3) implicated in bufadienolide resistance. Moreover, sequence motifs in ATP1A1 and ATP1A3 were predictive of bufadienolide resistance, suggesting that other mechanisms drive cane toad toxin susceptibility in C. johnstoni. We discuss alternative possible explanations for our observations based on crocodilian evolution, physiology, and other active components of toad toxin.