Abstract

Plutella xylostella (L.) has evolved resistance to various kinds of insecticide in the field. Reversion and selection, cross-resistance, inheritance and mechanisms of abamectin resistance were characterised in a field-derived multiresistant population of P. xylostella from China. Compared with a susceptible Roth strain, the field-derived TH population showed approximately 5000-fold resistance to abamectin. Rapid reversion of abamectin resistance was observed in the TH population when kept without insecticide selection. The TH-Abm strain, selected from the TH population with abamectin, developed 23 670-fold resistance to abamectin, a high level of cross-resistance to emamectin benzoate and low levels of cross-resistance to spinosad and fipronil. Genetic analyses indicated that abamectin resistance in the TH-Abm strain was autosomal, incompletely dominant and polygenic. P450 monooxygenase activities in the TH-Abm strain were significantly elevated compared with the TH strain. Piperonyl butoxide (PBO) inhibited a small part of abamectin resistance in the TH-Abm strain. Field-evolved high-level resistance to abamectin in the TH population was not stable. Selection of the TH population with abamectin resulted in an extremely high level of cross-resistance to emamectin benzoate and low levels of cross-resistance to spinosad and fipronil. Enhanced oxidative metabolism was involved in, but may not be the major mechanism of, polygenic abamectin resistance in the TH-Abm strain.

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