benzofurans and fufenozide

Although dibenzoylhydrazine-type non-steroidal ecdysone agonists, such as fufenozide, have an excellent performance record, the emergence of resistance could severely compromise the efficacy of these compounds in integrated pest management programs. To investigate possible mechanisms of resistance, we investigated the regulation of the expression of the PxEcR-B gene encoding the ecdysone receptor isoform B (PxEcR-B), which is the specific target of fufenozide in P. xylostella. Bioinformatics analysis revealed a putative miR-189942 binding site in the 3'-UTR of PxEcR-B mRNA. In a PxEcR-B 3'-UTR luciferase reporter system, miR-189942 downregulated the luciferase activity, and these effects were abolished by a deletion mutation in the putative miR-189942 binding site. Moreover, at 96 h after treatment with an agomir (mimic) or antagomir (inhibitor) of miR-189942, PxEcR-B expression was decreased by 71 ± 4% and increased by 4.19- fold respectively. Furthermore, overexpression or knockdown of miR-189942 changed the sensitivity of P. xylostella to fufenozide in vivo but had no influence on the sensitivity to chlorantraniliprole, which does not target PxEcR-B. These data indicate that miR-189942 suppressed PxEcR-B expression via binding at the 3'-UTR of PxEcR-B, thus increasing the tolerance of P. xylostella to fufenozide. These findings provide empirical evidence of the involvement of miRNAs in the regulation of insecticide resistance.

Topics: Animals; Benzofurans; Hydrazines; Insecticide Resistance; MicroRNAs; Moths; Protein Isoforms; Receptors, Steroid

Fufenozide is a novel non-steroidal ecdysone agonist with good efficacy against diamondback moth (DBM), Plutella xylostella (Lepidoptera: Plutellidae). At present, it is widely applied for the control of a range of lepidopterous pests in China. This study compared the activities of fufenozide and 12 other insecticides against unselected and fufenozide-selected strains of DBM to examine potential patterns of cross-resistance. The relative fitness of the fufenozide-selected strain was assessed to provide information pertinent to insecticide resistance management.. Compared with the susceptible strain (JSS), the fufenozide-resistant strain (JSR) showed high cross-resistance to dibenzoylhydrazines and benzoylphenylureas, low cross-resistance to abamectin and no cross-resistance to organophosphates, carbamates and pyrethroids. JSR had a lower reproductive ability and a relative fitness of 0.5 compared with JSS.. P. xylostella has the potential to develop resistance to fufenozide, albeit at the expense of fitness. Cross-resistance between the same and other classes of insecticides is of concern, and should be a key consideration when implementing fufenozide-based control strategies for this species.

Topics: Animals; Benzofurans; Female; Hydrazines; Insecticide Resistance; Insecticides; Life Cycle Stages; Male; Moths

The diamondback moth (DBM), Plutella xylostella (L.), is a cosmopolitan pest of cruciferous crops. Fufenozide, a novel non-steroidal ecdysone agonist, exhibits good efficacy and plays an increasingly important role in the control of Lepidopterous pests in China. A laboratory strain of DBM was selected for resistance to fufenozide, and the genetic basis of resistance was studied.. The resistant strain, selected under laboratory conditions, exhibited a higher level of resistance to fufenozide (302.8-fold based on LC(50)s) than the laboratory susceptible strain. Mortality data from the testing of F(1) progeny of reciprocal crosses of resistant and susceptible DBM indicated that resistance was autosomal and incompletely recessive with a degree of dominance of -0.664. Chi-square analysis from responses of a backcross of crossed F(1) progeny and the resistant strain and F(2) progeny were highly significant, suggesting that the resistance was probably controlled by more than one gene. The estimated realised heritability (h(2)) of fufenozide resistance was 0.08, indicating that diamondback moth may have a lower chance of developing resistance to fufenozide than other kinds of insecticide.. The resistance of DBM to fufenozide might be autosomal and incompletely recessive, and the resistance is probably controlled by more than one gene. These results provide the basic information for pest management programmes.

Topics: Animals; Benzofurans; Ecdysone; Female; Genes, Dominant; Hydrazines; Inheritance Patterns; Insecticide Resistance; Male; Moths