Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2009050 | Pesticide Biochemistry and Physiology | 2015 | 7 Pages |
•An isoline of the fall armyworm from Puerto Rico (PR) was highly resistant to Cry1F Bt toxin.•PR strain also developed 19-fold resistance to an organophosphate insecticide.•Mitochondrial COII sequencing revealed 2.8% molecular divergence between PR and susceptible strain.•Reduced gut alkaline phosphatase, aminopeptidase, and proteinase activities may be accounted for Bt resistance in PR strain.•Elevated esterase and glutathione S-transferase activities might be involved in detoxification of organophosphate insecticide.
Fall armyworm (FAW) is a damaging pest of many economic crops. Long-term use of chemical control prompted resistance development to many insecticide classes. Many populations were found to be significantly less susceptible to major Bt toxins expressed in transgenic crops. In this study, a FAW strain collected from Puerto Rico (PR) with 7717-fold Cry1F-resistance was examined to determine if it had also developed multiple/cross resistance to non-Bt insecticides. Dose response assays showed that the PR strain developed 19-fold resistance to acephate. Besides having a slightly smaller larval body weight and length, PR also evolved a deep (2.8%) molecular divergence in mitochondrial oxidase subunit II. Further examination of enzyme activities in the midgut of PR larvae exhibited substantial decreases of alkaline phosphatase (ALP), aminopeptidase (APN), 1-NA- and 2-NA-specific esterase, trypsin, and chymotrypsin activities, and significant increases of PNPA-specific esterase and glutathione S-transferase (GST) activities. When enzyme preparations from the whole larval body were examined, all three esterase, GST, trypsin, and chymotrypsin activities were significantly elevated in the PR strain, while ALP and APN activities were not significantly different from those of susceptible strain. Data indicated that multiple/cross resistances may have developed in the PR strain to both Bt toxins and conventional insecticides. Consistently reduced ALP provided evidence to support an ALP-mediated Bt resistance mechanism. Esterases and GSTs may be associated with acephate resistance through elevated metabolic detoxification. Further studies are needed to clarify whether and how esterases, GSTs, and other enzymes (such as P450s) are involved in cross resistance development to Bt and other insecticide classes.
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