The potential role of detoxification enzymes in diamide insecticide-resistant diamondback moth populations from Georgia, USA

The diamondback moth (DBM), Plutella xylostella, is a major pest of brassica crops that is prone to develop high levels of insecticide resistance. Research efforts in the Southeastern U.S. have primarily focused on the documentation of resistance outbreaks, most of which have been reliant on the toxicological characterization of field-populations via leaf-dip bioassays. Recently our lab began monitoring for known molecular mechanisms of insecticide resistance, resulting in the identification of the ryanodine receptor mutations I4790M, I4790K, and G4946E in populations from Georgia and Florida. While it seems likely that these mutations are major contributors to the observed diamide resistance in the region, other mechanisms are potentially contributing to resistance and should be explored. The detoxification of xenobiotics via specific enzymes is another mechanism of insecticide resistance that has been well studied in multiple insect species, including DBM. A variety of genes have been associated with chlorantraniliprole resistance across multiple gene families, including cytochrome P450s, UDP-glucuronosyltransferases, and carboxylesterases. In this study, we collected populations of DBM from different counties in Georgia, USA. After one generation in colony, each population was toxicologically characterized using the maximum labeled dose of chlorantraniliprole. Subsequently, larvae were exposed to a sublethal concentration of either chlorantraniliprole or methomyl for 24 hours. Using qPCR, we screened each population for the differential expression of genes of interest after exposure to sublethal concentrations of either active ingredient.