Characterisation of imidacloprid resistance in the bird cherry‐oat aphid, Rhopalosiphum padi, a serious pest on wheat crops. Issue 6 (8th February 2018)

• Record Type: Journal Article
• Authors: Wang, Kang; Zhang, Meng; Huang, Yanna; Yang, Zhuolin; Su, Sha; Chen, Maohua
• Is Part Of: Pest management science. Volume 74:Issue 6(2018)
• Page Start: 1457
• Page End: 1465
• Publication Date: 2018-02-08
• Subjects: Rhopalosiphum padi -- fitness -- cross‐resistance -- P450 -- nicotinic acetylcholine receptor (nAChR); Pests -- Control -- Periodicals; Pesticides -- Periodicals; 632.9
• DOI: 10.1002/ps.4834
• Languages: English
• ISSNs: 1526-498X

Abstract

Abstract: BACKGROUND: Rhopalosiphum padi is a destructive insect pest of wheat worldwide. Studies have shown that R. padi has developed resistance to different insecticides, including imidacloprid. We studied the mechanisms conferring resistance to imidacloprid at the biochemical and molecular levels. RESULTS: An R. padi imidacloprid‐resistant (IM‐R) strain and a susceptible (SS) strain were established. Fitness analysis using life‐tables showed that the IM‐R strain had obvious disadvantages in several parameters, indicating reduced fitness. Profiles of cross‐resistance of IM‐R and SS to seven insecticides were detected. Both synergistic and enzyme activity data suggested that P450 plays a role in resistance. Furthermore, the mRNA expression levels of cytochrome P450 (CYP) genes CYP6CY3‐1 and CYP6CY3‐2 were significantly increased in the IM‐R strain. No target‐site mutation within the nicotinic acetylcholine receptor (nAChR) subunits was detected in the IM‐R strain. Interestingly, the expression levels of the nAChR α1, α2, α3, α7‐2, and β1 subunit genes were significantly decreased, suggesting that down‐regulation of these subunits may be involved in resistance. CONCLUSION: Multiple mechanisms confer imidacloprid resistance in R. padi . © 2017 Society of Chemical Industry Abstract : Rhopalosiphum padi is a destructive insect pest of wheat crops worldwide. This article presents the mechanisms of resistance of the pest to imidacloprid at biochemical and molecular levels.