Nuclear factor erythroid-derived 2-related factor 2 activates glutathione S-transferase expression in the midgut of Spodoptera litura (Lepidoptera: Noctuidae) in response to phytochemicals and insecticides
Nuclear factor erythroid-derived 2-related factor 2 activates glutathione S-transferase expression in the midgut of Spodoptera litura (Lepidoptera: Noctuidae) in response to phytochemicals and insecticides
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DOI：
10.1111/imb.12391
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发表时间：
2018-08-01
影响因子：
2.6
通讯作者：
Zheng, S.
中科院分区：
文献类型：
--
作者：
Chen, S.;Lu, M.;Zheng, S.
解毒酶在昆虫对外源性化学物质如杀虫剂和植物化学物质的抗性中起重要作用。我们研究了激活谷胱甘肽S-转移酶（GST）的表达在选定的外源性物质的途径。通过对斜纹夜蛾GST 11（Slgste 1）基因启动子活性的分析，发现了一个顺式调控元件。一个抗氧化反应元件被激活，响应吲哚-3-甲醇（I3 C）和毒死蜱（CPF），并能够与异源生物传感器蛋白核因子红细胞衍生2相关因子2（SlNrf 2）结合。SlNrf 2和Slgste 1在斜纹夜蛾细胞系和斜纹夜蛾中肠中对I3 C和CPF诱导的活性氧应答。SlNrf 2 RNA干扰（RNAi）降低了Slgste 1的信使RNA水平和响应于I3 C、黄毒素、CPF和溴氰菊酯的GST的过氧化物酶活性。S1 Nrf 2 RNAi和GST活性的抑制剂处理降低了I3 C处理的细胞的活力。这些结果表明，SlNrf 2激活GST的表达，以响应由暴露于外源性物质引起的氧化应激。
Detoxication enzymes play an important role in insect resistance to xenobiotics such as insecticides and phytochemicals. We studied the pathway for activating the expression of glutathione S-transferases (GSTs) in response to selected xenobiotics. An assay of the promoter activity of GST epsilon 1 (Slgste1) of Spodoptera litura led to the discovery of a cis-regulating element. An antioxidant response element was activated in response to indole-3-carbinol (I3C) and chlorpyrifos (CPF) and was able to bind with the xenobiotic sensor protein nuclear factor erythroid-derived 2-related factor 2 (SlNrf2). SlNrf2 and Slgste1 were responsive to reactive oxygen species induced by I3C and CPF in a S.litura cell line, as well as in S.litura midguts. SlNrf2 RNA interference (RNAi) reduced the message RNA levels of Slgste1 and the peroxidase activity of GSTs in response to I3C, xanthotoxin, CPF and deltamethrin. SlNrf2 RNAi and inhibitor treatment of GST activity decreased the viability of I3C-treated cells. These results indicate that SlNrf2 activates the expression of GSTs in response to oxidative stresses caused by exposure to xenobiotics.