Cross‐resistance and biochemical mechanisms of abamectin resistance in the B‐type Bemisia tabaci

Abstract

Abstract: To understand the risk of resistance and the possible mechanisms of resistance to abamectin in B‐type Bemisia tabaci (Gennadius) better, a resistant strain of B. tabaci was selected in the laboratory and cross‐resistance pattern and resistance mechanisms to abamectin were investigated. The NJ‐Abm strain of B. tabaci was derived from a field population (NJ) collected in Nanjing, China in 2002 with 18 generations of selection with abamectin in the laboratory. Compared with the unselected NJ strain, the selected NJ‐Abm strain developed 14.5‐fold resistance to abamectin and showed significant cross‐resistance to emamectin benzoate (4.4‐fold) and imidacloprid (3.4‐fold), but no cross‐resistance to fipronil. The oxidase inhibitor piperonyl butoxide (PBO) and glutathione S‐transferase inhibitor diethyl maleate (DEM) produced significant synergism on abamectin in the NJ‐Abm strain (with synergistic ratios of 3.9‐ and 4.1‐fold respectively); however, the esterase inhibitor triphenyl phosphate (TPP) did not act synergistically with abamectin. Biochemical analysis confirmed that P450 monooxygenase activity and glutathione S‐transferase activity of the NJ‐Abm strain were elevated to 2.1‐ and 2.0‐fold, respectively, compared with that of the NJ strain. This indicated that enhanced metabolism mediated by P450 monooxygenase and glutathione S‐transferase is likely to be involved in abamectin resistance and cross‐resistance to imidacloprid and emamectin benzoate in the NJ‐Abm strain.