双酚enazate是一种新型杀螨剂,已广泛用于控制蜘蛛螨。有趣的是,我们发现联苯萘嗪对小菜蛾(小菜蛾)具有生物学活性,世界上十字花科作物上最重要的经济害虫之一。然而,小菜蛾对联苯萘嗪处理反应的分子机制尚不清楚。在这项研究中,我们首先估计了三龄P.xylostella幼虫的联苯萘嗪的LC30剂量。然后,为了确定对这种杀虫剂处理有反应的基因,比较转录组谱被用来分析暴露于联苯萘嗪LC30后,小菜蛾幼虫的基因表达变化。总的来说,757个差异表达基因(DEGs)在联苯钠处理和对照之间的小菜蛾幼虫被鉴定,其中526和231个基因上调和下调,分别。进一步的京都基因和基因组百科全书(KEGG)分析表明,外源生物代谢途径显着丰富,具有十个解毒酶基因(四个P450,五种谷胱甘肽S-转移酶(GSTs),和一个UDP-葡糖醛酸基转移酶(UGT)上调,并通过qRT-PCR验证了它们的表达模式。有趣的是,目前的结果表明,17个表皮蛋白(CP)基因也显著上调,包括15个CPR家族基因。此外,发现氧化磷酸化途径被激活,在联苯萘嗪处理的幼虫中,八个线粒体基因上调。相比之下,我们发现一些参与酪氨酸代谢和嘌呤通路的基因被下调,表明暴露于联苯萘嗪的幼虫的这两种途径被显着抑制。总之,本研究将有助于我们更好地了解亚致死剂量的联苯苄肼解毒和作用的分子机制。
Bifenazate is a novel acaricide that has been widely used to control spider mites. Interestingly, we found
bifenazate had a biological activity against the diamondback moth (Plutella xylostella), one of the most economically important pests on crucifer crops around the world. However, the molecular mechanisms underlying the response of P. xylostella to
bifenazate treatment are not clear. In this study, we first estimated the LC30 dose of
bifenazate for third-instar P. xylostella larvae. Then, in order to identify genes that respond to the treatment of this insecticide, the comparative transcriptome profiles were used to analyze the gene expression changes in P. xylostella larvae after exposure to LC30 of bifenazate. In total, 757 differentially expressed genes (DEGs) between
bifenazate-treated and control P. xylostella larvae were identified, in which 526 and 231 genes were up-regulated and down-regulated, respectively. The further Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the xenobiotics metabolisms pathway was significantly enriched, with ten detoxifying enzyme genes (four P450s, five glutathione S-transferases (GSTs), and one UDP-Glucuronosyltransferase (UGT)) were up-regulated, and their expression patterns were validated by qRT-PCR as well. Interestingly, the present results showed that 17 cuticular protein (CP) genes were also remarkably up-regulated, including 15 CPR family genes. Additionally, the oxidative phosphorylation pathway was found to be activated with eight mitochondrial genes up-regulated in bifenazate-treated larvae. In contrast, we found some genes that were involved in tyrosine metabolism and purine pathways were down-regulated, indicating these two pathways of bifenazate-exposed larvae were significantly inhibited. In conclusion, the present study would help us to better understand the molecular mechanisms of sublethal doses of bifenazate detoxification and action in P. xylostella.