Naoya Sugimoto1, Masahiro Osakabe. 1. Laboratory of Ecological Information, Graduate School of Agriculture, Kyoto University, Kyoto, Japan.
Abstract
BACKGROUND: Cyenopyrafen is an inhibitor of complex II of the mitochondrial electron transport chain. It has a molecular structure that shares some common features with frequently used complex I inhibitors such as pyridaben. To evaluate whether this similarity in structure poses a cross-resistance risk that might complicate resistance management, we selected for pyridaben and cyenopyrafen resistance in the laboratory and characterized resistance. RESULTS: The selection for cyenopyrafen conferred cross-resistance to pyridaben and vice versa. Resistance towards these both acaricides was incompletely dominant in adult females. However, in eggs maternal effects were observed in pyridaben resistance, but not in the cyenopyrafen-resistance (completely dominant). In the cyenopyrafen resistant strain, the LC50 of eggs remained lower than the commercially recommended concentration. The common detoxification mechanisms by cytochrome P450 was involved in resistance to these acaricides. Carboxyl esterases were also involved in cyenopyrafen resistance as a major factor. CONCLUSIONS: Although cross-resistance suggests that pyridaben resistance would confer cyenopyrafen cross-resistance, susceptibility in eggs functions to delay the development of cyenopyrafen resistance.
BACKGROUND:Cyenopyrafen is an inhibitor of complex II of the mitochondrial electron transport chain. It has a molecular structure that shares some common features with frequently used complex I inhibitors such as pyridaben. To evaluate whether this similarity in structure poses a cross-resistance risk that might complicate resistance management, we selected for pyridaben and cyenopyrafen resistance in the laboratory and characterized resistance. RESULTS: The selection for cyenopyrafen conferred cross-resistance to pyridaben and vice versa. Resistance towards these both acaricides was incompletely dominant in adult females. However, in eggs maternal effects were observed in pyridaben resistance, but not in the cyenopyrafen-resistance (completely dominant). In the cyenopyrafen resistant strain, the LC50 of eggs remained lower than the commercially recommended concentration. The common detoxification mechanisms by cytochrome P450 was involved in resistance to these acaricides. Carboxyl esterases were also involved in cyenopyrafen resistance as a major factor. CONCLUSIONS: Although cross-resistance suggests that pyridaben resistance would confer cyenopyrafen cross-resistance, susceptibility in eggs functions to delay the development of cyenopyrafen resistance.