报告摘要: Animal adaptation to voltage-gated Na+ channel blockers (STX, TTX) has proven to be a fruitful system for understanding predator-prey dynamics and trophic transfer in food webs, and molecular adaptation. Resistance to these toxins has been linked to mutations in the toxin-binding region of the Na+channel that dramatically decrease toxin-binding affinity. Here, we report a novel, and apparently common, mutation in a marine copepod located near the inactivation gate of the Na+ channel, which leads to persistent Na+ currents when the channel is inactivated; i.e., a leaky Na+ channel. Leaky channels result in unintended action potentials, and cell hypersensitivity to sub-threshold stimuli; hence, they are presumed to be costly to individuals. However, we demonstrate a positive effect of STX on heterozygous copepods bearing this mutation. This positive response is consistent with a simple genetic system in which heterozygotes are advantaged. This novel mechanism of adaptation to neurotoxins has profound implications for the fate of toxic phytoplankton blooms and for understanding adaptive responses of grazers.
