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首页> 外文期刊>Journal of Agricultural and Food Chemistry >Phytochemical Flavone Confers Broad-Spectrum Tolerance to Insecticides in Spodoptera litura by Activating ROS/CncC-Mediated Xenobiotic Detoxification Pathways
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Phytochemical Flavone Confers Broad-Spectrum Tolerance to Insecticides in Spodoptera litura by Activating ROS/CncC-Mediated Xenobiotic Detoxification Pathways

机译：通过激活ROS / CNCC介导的异卵戒毒途径，植物化学性黄酮对Spodoptera Litura的杀虫剂赋予杀虫剂的广谱耐受性

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Tolerance to chemical insecticides can be driven by the necessity of herbivorous insects to defend against host plant-produced phytochemicals. However, how the phytochemicals are sensed and further transduced into a defense response associated with insecticide tolerance is poorly understood. Herein, we show that pre-exposure to flavone, a flavonoid phytochemical, effectively enhanced larval tolerance to multiple synthetic insecticides and elevated detoxification enzyme activities in Spodoptera litura. RNASeq analysis revealed that flavone induced a spectrum of genes spanning phase I and II detoxification enzyme families, as well as two transcription factors Cap "n" collar isoform C (CncC) and its partner small muscle aponeurosis fibromatosis (MafK). Knocking down of CncC by RNA interference suppressed flavone-induced detoxification gene expression and rendered the larvae more sensitive to the insecticides. Flavone exposure elicited a reactive oxygen species (ROS) burst, while scavenging of ROS inhibited CncC-mediated detoxification gene expression and suppressed flavone-induced detoxification enzyme activation. Metabolome analysis showed that the ingested flavone was mainly converted into three flavonoid metabolites, and only 3-hydroxyflavone was found to affect the ROS/CncC pathway-mediated metabolic detoxification. These results indicate that the ROS/CncC pathway is an important route driving detoxification gene expression responsible for insecticide tolerance after exposure to the phytochemical flavone.
机译：对化学杀虫剂的耐受性可以由食草动物抵御寄主植物产生的植物化学物质的必要性驱动。然而，人们对这些植物化学物质如何被感知并进一步转化为与杀虫剂耐受性相关的防御反应知之甚少。在此，我们表明，预先暴露于黄酮类植物化学物质黄酮，可有效增强斜纹夜蛾幼虫对多种合成杀虫剂的耐受性，并提高解毒酶活性。RNASeq分析显示，黄酮诱导了一系列跨越I期和II期解毒酶家族的基因，以及两种转录因子Cap“n”领亚型C（CncC）及其伴侣小肌肉腱膜纤维瘤病（MafK）。RNA干扰击倒CncC抑制了黄酮诱导的解毒基因表达，使幼虫对杀虫剂更敏感。黄酮暴露引起活性氧（ROS）爆发，而清除ROS抑制CncC介导的解毒基因表达，抑制黄酮诱导的解毒酶激活。代谢组学分析表明，摄入的黄酮主要转化为三种黄酮代谢产物，只有3-羟基黄酮影响ROS/CncC途径介导的代谢解毒。这些结果表明，ROS/CncC途径是一条重要的途径，在暴露于植物化学物质黄酮后驱动解毒基因的表达，该基因与杀虫剂耐受性有关。

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