Characterizing genetic variation associated with imidacloprid resistance from multiple geographic populations of the Colorado potato beetle

The Colorado potato beetle (CPB), Leptinotarsa decemlineata (Coleoptera: Chrysomelidae), is an agricultural super-pest largely attributed to its extraordinary ability to develop insecticide resistance. Neonicotinoids have successfully controlled CPB for nearly 30 years; however, an increased neonicotinoid tolerance is observed across CPB populations. Overexpression of metabolic enzymes plays an essential role in CPB neonic resistance, while amino acid changes of proteins may also involve. Genetic modification on the insecticide target site can prevent insecticide binding or interaction at its site of action, thereby reducing or eliminating the toxicity of the insecticide, and mutations on metabolic enzymes can alter their metabolic capacity leading to enhanced detoxification. Here, I report variation between imidacloprid resistance and susceptible CPB populations from a panel of resistant candidate genes. These genes are known or hypothesized to be involved in imidacloprid resistance of CPB, including genes encoding nicotinic acetylcholine receptors, the neonicotinoid target site, and genes encoding metabolic enzymes, such as P450 and GSTs. Mutations that occur more frequently in resistant than susceptible beetles and result in structural changes of protein sequence were regarded as associated with imidacloprid resistance.