Neonicotinoid insecticides induce salicylate-associated plant defense responses
Neonicotinoid insecticides induce salicylate-associated plant defense responses
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DOI：
10.1073/pnas.1013020107
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发表时间：
2010-10-12
影响因子：
11.1
通讯作者：
Wildermuth, Mary C.
中科院分区：
文献类型：
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作者：
Ford, Kevin A.;Casida, John E.;Wildermuth, Mary C.
新烟碱类杀虫剂基于它们作为昆虫烟碱型乙酰胆碱受体激动剂的作用来控制作物害虫，该受体几乎同样能接受氯吡啶和氯噻唑类似物。在某些情况下，这些化合物也被报道增强植物活力和(A)生物抗逆性，不依赖于它们的杀虫功能。然而，这种行动模式还没有定义。以拟南芥为材料，我们发现新烟碱类化合物吡虫啉(IMI)和氯硫醚(CLO)分别通过它们的6-氯吡啶-3-羧酸和2-氯噻唑-5-羧酸代谢产物诱导水杨酸(SA)相关的植物反应。SA是一种植物激素，因其在植物防御病原菌和诱导系统获得性抗性中的作用而闻名；然而，它也可以调节非生物胁迫反应。这些新烟碱类化合物的全球转录反应与SA相似，包括与(A)生物应激反应有关的基因。此外，与SA类似，IMI和CLO诱导系统获得抗性，导致白粉病病原菌生长减少。ClO的作用通过SA生物合成酶ICS1诱导SA的内源合成，ICS1是ClO诱导SA积累、SA标记PR1表达和充分提高对白粉病抗性所必需的ICS1。相反，IMI的作用并不诱导SA的内源性合成。相反，IMI进一步被激活为6-氯-2-羟基吡啶基-3-羧酸，这是一种有效的PR1诱导剂和SA敏感酶的抑制物。因此，通过不同的机制，这些氯吡啶基和氯噻唑基新烟碱诱导SA反应与增强的应激耐受性有关。
Neonicotinoid insecticides control crop pests based on their action as agonists at the insect nicotinic acetylcholine receptor, which accepts chloropyridinyl- and chlorothiazolyl-analogs almost equally well. In some cases, these compounds have also been reported to enhance plant vigor and (a) biotic stress tolerance, independent of their insecticidal function. However, this mode of action has not been defined. Using Arabidopsis thaliana, we show that the neonicotinoid compounds, imidacloprid (IMI) and clothianidin (CLO), via their 6-chloropyridinyl-3-carboxylic acid and 2-chlorothiazolyl-5-carboxylic acid metabolites, respectively, induce salicylic acid (SA)-associated plant responses. SA is a phytohormone best known for its role in plant defense against pathogens and as an inducer of systemic acquired resistance; however, it can also modulate abiotic stress responses. These neonicotinoids effect a similar global transcriptional response to that of SA, including genes involved in (a) biotic stress response. Furthermore, similar to SA, IMI and CLO induce systemic acquired resistance, resulting in reduced growth of a powdery mildew pathogen. The action of CLO induces the endogenous synthesis of SA via the SA biosynthetic enzyme ICS1, with ICS1 required for CLO-induced accumulation of SA, expression of the SA marker PR1, and fully enhanced resistance to powdery mildew. In contrast, the action of IMI does not induce endogenous synthesis of SA. Instead, IMI is further bioactivated to 6-chloro-2-hydroxypyridinyl-3-carboxylic acid, which is shown here to be a potent inducer of PR1 and inhibitor of SA-sensitive enzymes. Thus, via different mechanisms, these chloropyridinyl- and chlorothiazolyl-neonicotinoids induce SA responses associated with enhanced stress tolerance.