Effects of Bacillus thuringiensis Treatment on Expression of Detoxification Genes in Chlorantraniliprole-Resistant Plutella xylostella.

Simple Summary: Detoxification genes play a crucial role in insect resistance to chemical pesticides, and exposure to biopesticides such as Bacillus thuringiensis (Bt) can modify their expression. Chlorantraniliprole (CAP)-resistant diamondback moth strains from China showed different expression of the detoxification genes tested (GST1, CYP6B7, and CarE-6) after treatment with CAP and Bt pesticides. The upregulation of CYP6B7 was observed after exposure to CAP, while the same gene was downregulated after larvae were exposed to Bt. Downregulation of CYP6B7 using RNAi without pretreatment with Bt resulted in increased susceptibility to CAP in resistant DBM strains, signifying a contribution of this gene to the resistant phenotype. Detoxification genes are crucial to insect resistance against chemical pesticides, yet their expression may be altered by exposure to biopesticides such as spores and insecticidal proteins of Bacillus thuringiensis (Bt). Increased enzymatic levels of selected detoxification genes, including glutathione S-transferase (GST), cytochrome P450 (CYP450), and carboxylesterase (CarE), were detected in chlorantraniliprole (CAP)-resistant strains of the diamondback moth (DBM, Plutella xylostella) from China when compared to a reference susceptible strain. These CAP-resistant DBM strains displayed distinct expression patterns of GST 1, CYP6B7, and CarE-6 after treatment with CAP and a Bt pesticide (Bt-G033). In particular, the gene expression analysis demonstrated significant upregulation of the CYP6B7 gene in response to the CAP treatment, while the same gene was downregulated following the Bt-G033 treatment. Downregulation of CYP6B7 using RNAi resulted in increased susceptibility to CAP in resistant DBM strains, suggesting a role of this gene in the resistant phenotype. However, pretreatment with a sublethal dose of Bt-G033 inducing the downregulation of CYP6B7 did not significantly increase CAP potency against the resistant DBM strains. These results identify the DBM genes involved in the metabolic resistance to CAP and demonstrate how their expression is affected by exposure to Bt-G033. [ABSTRACT FROM AUTHOR]