Abstract

UDP-glycosyltransferases (UGTs), as phase II detoxification enzymes, are widely distributed within living organisms and play vital roles in the biotransformation of endobiotics and xenobiotics in insects. Insects increase the expression of detoxification enzymes to cope with the stress of xenobiotics, including insecticides. However, the roles of UGTs in insecticide resistance are still seldom reported. In this study, two UGT inhibitors, namely, 5-nitrouracil and sulfinpyrazone, were found to synergistically increase the toxicity of imidacloprid in the resistant population of Diaphorina citri. Based on transcriptome data, a total of 17 putative UGTs were identified. Quantitative real-time PCR showed that fourteen of the 17 UGT genes were overexpressed in the resistant population relative to the susceptible population. Using RNA interference technology to knockdown six UGT genes, the results suggested that silencing the selected UGT375A1, UGT383A1, UGT383B1, and UGT384A1 genes dramatically increased the toxicity of imidacloprid in the resistant population. However, silencing the UGT362B1 and UGT379A1 genes did not result in a significant increase in the toxicity of imidacloprid in the resistant population. These findings revealed that some upregulated UGT genes were involved in imidacloprid resistance in D. citri. These results shed some light upon and further our understanding of the mechanisms of insecticide resistance in insects.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.