Génétique et Evolution des Maladies Infectieuses, CNRS, UMR 2724, Centre de Recherche IRD, 911 Avenue Agropolis, 34394 Montpellier, France.
J Med Entomol. 2011 May;48(3):694-700. doi: 10.1603/me10121.
The extensive use of insecticides to control vector populations has lead to the widespread development of different mechanisms of insecticide resistance. Mutations that confer insecticide resistance are often associated to fitness costs that prevent them from spreading to fixation. In vectors, such fitness costs include reductions in preimaginal survival, adult size, longevity, and fecundity. The most commonly invoked explanation for the nature of such pleiotropic effects of insecticide resistance is the existence of resource-based trade-offs. According to this hypothesis, insecticide resistance would deplete the energetic stores of vectors, reducing the energy available for other biological functions and generating trade-offs between insecticide resistance and key life history traits. Here we test this hypothesis by quantifying the energetic resources (lipids, glycogen, and glucose) of larvae and adult females of the mosquito Culex pipiens L. resistant to insecticides through two different mechanisms: esterase overproduction and acetylcholinesterase modification. We find that, as expected from trade-off theory, insecticide resistant mosquitoes through the overproduction of esterases contain on average 30% less energetic reserves than their susceptible counterparts. Acetylcholinesterase-modified mosquitoes, however, also showed a significant reduction in energetic resources (20% less). We suggest that, in acetylcholinesterase-modified mosquitoes, resource depletion may not be the result of resource-based trade-offs but a consequence of the hyperactivation of the nervous system. We argue that these results not only provide a mechanistic explanation for the negative pleiotropic effects of insecticide resistance on mosquito life history traits but also can have a direct effect on the development of parasites that depend on the vector's energetic reserves to fulfil their own metabolic needs.
为了控制病媒种群，人们广泛使用杀虫剂，这导致了不同杀虫剂抗性机制的广泛发展。赋予杀虫剂抗性的突变通常与适应度成本相关，这些成本会阻止它们传播到固定状态。在病媒中，这些适应度成本包括预蛹存活率、成虫大小、寿命和繁殖力降低。对于杀虫剂抗性的这种多效性影响的本质，最常被援引的解释是存在基于资源的权衡。根据这一假设，杀虫剂抗性会耗尽病媒的能量储备，减少用于其他生物学功能的能量，并在杀虫剂抗性和关键生活史特征之间产生权衡。在这里，我们通过量化对杀虫剂具有两种不同抗性机制（酯酶过度表达和乙酰胆碱酯酶修饰）的蚊子 Culex pipiens L. 的幼虫和雌性成虫的能量资源（脂质、糖原和葡萄糖）来检验这一假设。我们发现，正如权衡理论所预期的那样，通过过度表达酯酶产生抗性的蚊子平均比敏感型蚊子的能量储备少 30%。然而，乙酰胆碱酯酶修饰的蚊子也表现出显著的能量资源减少（少 20%）。我们认为，在乙酰胆碱酯酶修饰的蚊子中，资源枯竭可能不是基于资源的权衡的结果，而是神经系统过度激活的结果。我们认为，这些结果不仅为杀虫剂抗性对蚊子生活史特征的负面影响提供了一种机制解释，而且对依赖媒介的能量储备来满足自身代谢需求的寄生虫的发展也有直接影响。
