Laboratory of Neurogenetics and Behavior, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Laboratory of Neurogenetics and Behavior, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA; Kavli Neural Systems Institute, 1230 York Avenue, New York, NY 10065, USA; Howard Hughes Medical Institute, 1230 York Avenue, New York, NY 10065, USA.
Curr Biol. 2019 May 6;29(9):1551-1556.e5. doi: 10.1016/j.cub.2019.04.004. Epub 2019 Apr 25.
DEET (N, N-diethyl-meta-toluamide) is the most effective and widely used insect repellent, but its mechanism of action is both complex and controversial [1]. DEET acts on insect smell [2-6] and taste [7-11], and its olfactory mode of action requires the odorant co-receptor orco [2, 3, 6]. We previously observed that orco mutant female Aedes aegypti mosquitoes are strongly attracted to humans even in the presence of DEET, but they are rapidly repelled after contacting DEET-treated skin [6]. DEET inhibits food ingestion by Drosophila melanogaster flies, and this repellency is mediated by bitter taste neurons in the proboscis [9]. Similar neurons were identified in the mosquito proboscis, leading to the hypothesis that DEET repels on contact by activating an aversive bitter taste pathway [10]. To understand the basis of DEET contact chemorepellency, we carried out behavioral experiments and discovered that DEET acts by three distinct mechanisms: smell, ingestion, and contact. Like bitter tastants, DEET is a feeding deterrent when ingested, but its bitterness per se does not fully explain DEET contact chemorepellency. Mosquitoes blood fed on human arms treated with high concentrations of bitters, but rapidly avoided DEET-treated skin and did not blood feed. Insects detect tastants both through their proboscis and legs. We show that DEET contact chemorepellency is mediated exclusively by the tarsal segments of the legs and not the proboscis. This work establishes mosquito legs as the behaviorally relevant contact sensors of DEET. These results will inform the search for molecular mechanisms mediating DEET contact chemorepellency and novel contact-based insect repellents.
避蚊胺（N，N-二乙基-间-甲苯酰胺）是最有效和广泛使用的昆虫驱避剂，但它的作用机制既复杂又有争议[1]。避蚊胺作用于昆虫的嗅觉[2-6]和味觉[7-11]，其嗅觉作用模式需要气味受体或 co [2, 3, 6]。我们之前观察到，orco 突变的雌性埃及伊蚊即使在避蚊胺存在的情况下也会强烈吸引人类，但在接触到用避蚊胺处理过的皮肤后，它们会迅速被驱避[6]。避蚊胺抑制黑腹果蝇的食物摄入，这种驱避作用是由喙中的苦味神经元介导的[9]。在蚊子的喙中也鉴定出了类似的神经元，这导致了一个假设，即避蚊胺通过激活厌恶的苦味通路来触发性驱避[10]。为了了解避蚊胺接触驱避的基础，我们进行了行为实验，发现避蚊胺通过三种不同的机制起作用：嗅觉、摄入和接触。像苦味味觉剂一样，避蚊胺在摄入时是一种摄食抑制剂，但它的苦味本身并不能完全解释避蚊胺的接触驱避作用。蚊子在吸食高浓度苦味剂处理过的人的手臂上的血液，但会迅速避开用避蚊胺处理过的皮肤，并且不吸血。昆虫通过它们的喙和腿来检测味觉剂。我们表明，避蚊胺的接触驱避性完全是由腿部的跗节介导的，而不是喙。这项工作将蚊子的腿确定为避蚊胺的行为相关接触传感器。这些结果将为寻找介导避蚊胺接触驱避性的分子机制和新型接触式昆虫驱避剂提供信息。
