Analysis of translation control tumor protein related to deltamethrin stress in Drosophila kc cells
文献类型: 外文期刊
作者: Ying, Xiaoli 1 ; Liu, Yahui 1 ; Chen, Lu 1 ; Bo, Qian 1 ; Xu, Qin 3 ; Li, Fengliang 2 ; Zhou, Changfa 1 ; Cheng, Luogen 1 ;
作者机构: 1.Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Biodivers & Biotechnol, Nanjing 210023, Jiangsu, Peoples R China
2.Guizhou Acad Agr Sci, Inst Plant Protect, Guiyang 550009, Guizhou, Peoples R China
3.Nanjing Normal Univ, Sch Energy & Mech Engn, Nanjing 210042, Jiangsu, Peoples R China
关键词: TCTP; Drosophila kc cells; Deltamethrin; Stress; Resistance
期刊名称:CHEMOSPHERE ( 影响因子:7.086; 五年影响因子:6.956 )
ISSN: 0045-6535
年卷期: 2019 年 231 卷
页码:
收录情况: SCI
摘要: The translation control tumor protein (TCTP) is a kind of conservative, common and important molecule, several functions (such as regulating cell cycle, apoptosis and calcium binding) have been reported. However, few academic researches for role of TCTP in insecticides stress were made so far. In this research, Drosophila kc cells treated with different doses of deltamethrin at different times, indicated that the expression of TCTP reached the highest level when the cells were treated with 20 ppm of deltamethrin at 24 h. The results showed that TCTP expression is associated with deltamethrin stress. To investigate the functional relationship between this gene and deltamethrin resistance, RNA interference (RNAi) and cell transfection were utilized. TCTP knockdown significantly reduced the level of resistance of RNAi-treated cells, and the overexpressions of TCTP in Drosophila kc cells conferred a degree of protection against deltamethrin. Flow cytometry data showed increased apoptosis rate of RNAi-treated cells and decreased apoptosis following cell transfection. These results represent the first evidence that TCTP plays an important role in the regulation of deltamethrin resistance. Therefore, this study could help us to elucidate the environmental toxicity of deltamethrin and new target genes associated with resistance. (C) 2019 Elsevier Ltd. All rights reserved.
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