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The diamondback moth Plutella xylostella (L.) (Lepidoptera: Plutellidae) is a devastating pest that infests several cruciferous vegetable crops worldwide and has developed insecticide resistance in most chemical classes. Fluxametamide is a novel neuroactive isoxazoline compound that binds to a unique site on the γ -aminobutyric acid (GABA) receptor and has an exceptional insecticidal activity on a range of lepidopteran caterpillars. The present study aimed to assess the risk of resistance in P. xylostella to fluxametamide under laboratory conditions. After the repeated exposure to fluxametamide for successive 18 generations of P. xylostella , there was 3.095-fold increase in the LC 50. When the realized heritability (h 2 ) of P. xylostella to fluxametamide in the open field was assumed to be the laboratory-estimated value (h 2 = 0.180) and the mortality was 70–90%, only 22.9–33.1 generations were expected to be required to obtain a 10-fold increase in fluxametamide resistance. Compared with the laboratory susceptible strain (F 0), the Flux-SEL (F 18) strain exhibited a very low level of cross-resistance to emamectin benzoate (5.17-fold) and no significant cross-resistance to fipronil or flubendiamide. With the F 0 and the Flux-SEL test strains (F 12 , F 15 and F 18), the specific activities of cytochrome P450 and glutathione S -transferase showed a remarkable increase during selection, while the esterase activity did not differ significantly. The results indicated that a potential risk of resistance development to fluxametamide exists in P. xylostella after continuous exposure. These pieces of information will be crucial in formulating rational fluxametamide application and resistance management guidelines for controlling P. xylostella under field condition. [Display omitted] • First report of laboratory-selected fluxametamide resistance in Plutella xylostella. • P. xylostella carries a potential risk of field-evolved resistance to fluxametamide. • The estimated h 2 of fluxametamide resistance in Flux-SEL (F 18) strain was 0.180. • Flux-SEL (F 18) strain was weakly resistant to emamectin benzoate. • The activities of P450 and GST increased significantly in Flux-SEL strains during selection. [ABSTRACT FROM AUTHOR]

The cotton whitefly, Bemisia tabaci (Gennadius) is a devastating polyphagous insect pest worldwide and has been shown to be resistant to insecticides in most chemical classes. The newly commercialized pyropene insecticide afidopyropen provided a new tool to control B. tabaci because of high selectivity and its novel mode of action. This study aimed to evaluate the susceptibility of B. tabaci Asia I from ten provinces of India to afidopyropen and other commonly used insecticides. Most field-collected populations were susceptible to afidopyropen, with LC 50 values varying from 4.37 to 16.62 mg L−1. However, four field populations (W-MH, K-UP, M-WB and L-PN) exhibited moderate levels of resistance (28.53, 19.09, 35.27 and 30.81-fold, respectively), but no cross-resistance to cyantraniliprole and pymetrozine. Diethyl maleate (DEM) significantly restored the susceptibility of W-MH, M-WB and L-PN strains of B. tabaci to afidopyropen, whereas piperonyl butoxide (PBO) significantly inhibited afidopyropen resistance in K-UP, M-WB and L-PN populations. The activities of glutathione S -transferase (GST) and P450 monooxygenase increased in the afidopyropen-resistant field strains, while esterase activity did not change significantly. The present study showed a regional variation in afidopyropen toxicities among B. tabaci Asia I populations from different agro-climatic zones of India, which suggests a potential risk of afidopyropen resistance development. Metabolic detoxification mediated by GST and P450 monooxygenase was associated with afidopyropen resistance in B. tabaci Asia I. [Display omitted] • First report of afidopyropen resistance in Bemisia tabaci Asia I. • Four field-strains exhibited moderate level of resistance. • No cross-resistance of afidopyropen with cyantraniliprole or pymetrozine. • Elevated GST and P450 activities in afidopyropen-resistant populations. [ABSTRACT FROM AUTHOR]