MiR-189942 regulates fufenozide susceptibility by modulating ecdysone receptor isoform B in Plutella xylostella (L.)

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.