All animals must detect noxious stimuli to initiate protective behavior, but the evolutionary origin of nociceptive systems is not well understood. Here we show that noxious heat and irritant chemicals elicit robust escape behaviors in the planarian Schmidtea mediterranea and that the conserved ion channel TRPA1 is required for these responses. TRPA1-mutant Drosophila flies are also defective in noxious-heat responses. We find that either planarian or human TRPA1 can restore noxious-heat avoidance to TRPA1-mutant Drosophila, although neither is directly activated by heat. Instead, our data suggest that TRPA1 activation is mediated by H₂O₂ and reactive oxygen species, early markers of tissue damage rapidly produced as a result of heat exposure. Together, our data reveal a core function for TRPA1 in noxious heat transduction, demonstrate its conservation from planarians to humans, and imply that animal nociceptive systems may share a common ancestry, tracing back to a progenitor that lived more than 500 million years ago.

中文翻译：

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活性氧对涡虫 TRPA1 的激活揭示了动物伤害感受的保守机制。

所有动物都必须检测到有害刺激才能启动保护行为，但伤害感受系统的进化起源尚不清楚。在这里，我们发现有毒的热量和刺激性化学物质会引起涡虫 Schmidtea mediterranea 的强烈逃逸行为，并且这些反应需要保守的离子通道 TRPA1。TRPA1 突变的果蝇在有害热反应方面也存在缺陷。我们发现涡虫或人类 TRPA1 都可以恢复 TRPA1 突变果蝇的热回避能力，尽管两者都不是直接被热激活的。相反，我们的数据表明 TRPA1 激活是由 H ₂ O ₂和活性氧介导的，它们是由于热暴露而迅速产生的组织损伤的早期标志。总之，我们的数据揭示了TRPA1在有害热传导中的核心功能，证明了其从涡虫到人类的保守性，并暗示动物伤害感受系统可能具有共同的祖先，可以追溯到生活在5亿多年前的祖先。