Genetics and evidence for an esterase-associated mechanism of resistance to indoxacarb in a field population of diamondback moth (Lepidoptera: Plutellidae)

Bioassays (at generation G(2)) with a newly collected field population (designated CH3) of Plutella xylostella L. from farmers' fields in the Cameron Highlands, Malaysia, indicated resistance ratios of 813-, 79-, 171-, 498- and 1285-fold for indoxacarb, fipronil, spinosad, deltamethrin and Bacillus thuringiensis toxin Cry1Ac respectively compared with a laboratory susceptible population (Lab-UK). At G(2) the field-derived population was divided into two subpopulations: one was selected (G(2) to G(7)) with indoxacarb (indoxa-SEL), while the second was left unselected (UNSEL). A significant reduction in the resistance ratio for each compound was observed in UNSEL at G(8). For indoxa-SEL, bioassays at G(8) found that selection with indoxacarb gave a resistance ratio of 2594 compared with Lab-UK and of 90 compared with UNSEL. The toxicity of fipronil, spinosad and deltamethrin was not significantly different in indoxa-SEL at G(8) compared with G(2) but was significantly greater than UNSEL at G(8). The toxicity of Cry1Ac was significantly reduced in indoxa-SEL at G(8) compared with G(2) but was also significantly greater than UNSEL at G(8). This suggests that indoxacarb selection maintained resistance to these compounds in the indoxa-SEL population. Synergist studies indicated that resistance to indoxacarb in indoxa-SEL was esterase associated. Logit regression analysis of F, reciprocal crosses between indoxa-SEL and Lab-UK indicated that resistance to indoxacarb was inherited as an autosomal, incompletely recessive (D-LC = 0.35) trait. Tests of monogenic inheritance suggested that resistance to indoxacarb was controlled by a single locus. (c) 2006 Society of Chemical Industry.