Functional analysis of a point mutation in the ryanodine receptor of Plutella xylostella (L.) associated with resistance to chlorantraniliprole

• DOI: 10.1002/ps.3651
• Publication Date: 2013-09-13T08:12:21Z
• Authors: Lei Guo; Yi Wang; Xuguo Zhou; Zhenyu Li; Shangzhong Liu; Liang Pei; Xiwu Gao
• Keywords: Insecticide Resistance; Insecticides; 0303 health sciences; 03 medical and health sciences; Amino Acid Substitution; Animals; Point Mutation; Ryanodine Receptor Calcium Release Channel; ortho-Aminobenzoates; Moths

AbstractBACKGROUNDThe diamondback moth, Plutella xylostella (L.) has developed extremely high resistance to chlorantraniliprole and other diamide insecticides in the field. A glycine to glutamic acid substitution (G4946E) in the P. xylostella ryanodine receptor (PxRyR) has been found in two resistant populations collected in Thailand and Philippines and was considered associated with the diamide insecticides resistance but no experimental evidence was provided. The present study aimed to clarify the function of the reported mutation in chlorantraniliprole resistance in P. xylostella.RESULTSWe identified the same mutation (G4946E) in PxRyR from four field collected chlorantraniliprole resistant populations of Plutella xylostella in China. Most importantly, we found that the frequency of the G4946E mutation is significantly correlated to the chlorantraniliprole resistance ratios in P. xylostella (R2 = 0.82, P = 0.0003). Ligand binding assays showed that the binding affinities of the PxRyR to the chlorantraniliprole in three field resistant populations were 2.41‐, 2.54‐ and 2.60‐times lower than that in the susceptible one.CONCLUSIONFor the first time we experimentally proved that the G4946E mutation in PxRyR confers resistance to chlorantraniliprole in Plutella xylostella. These findings pave the way for the complete understanding of the mechanisms of diamide insecticides resistance in insects. © 2013 Society of Chemical Industry