Role of miR-276-3p in the cyantraniliprole resistance mechanism of Bemisia tabaci via CYP6CX3 targeting

Abstract

The sweet potato whitefly, Bemisia tabaci, is an important insect pest that transmits over 200 different plant viruses and causes serious damage to the production of cotton and Solanaceae vegetables. Cyantraniliprole is the first diamide insecticide, showing toxicity against B. tabaci. However, B. tabaci has developed resistance to this insecticide by upregulating the expressions of cytochrome P450 genes such as CYP6CX3, while there is limited information on the regulatory mechanism mediated by miRNA. In the present study, ten miRNAs were predicted to target CYP6CX3, in which miR-276-3p showed an inverse expression pattern with CYP6CX3 in two cyantraniliprole resistant strains and under cyantraniliprole exposure. A luciferase assay demonstrated that miR-276-3p suppressed CYP6CX3 expression by pairing with residues 1445–1453. Overexpression or knockdown of miR-276-3p directly impacted B. tabaci resistance to cyantraniliprole. In addition, exposure to cyantraniliprole led to a significant reduction in the expressions of five genes (drosha, dicer1, dicer2, Ago1, and Ago2A) associated with miRNA biogenesis. Suppressing genes such as drosha, dicer1, and Ago2A reduced the expression of miR-276-3p, increased CYP6CX3 expression, and decreased B. tabaci resistance to cyantraniliprole. These results improve our understanding of the role of miRNAs in P450 regulation and cyantraniliprole resistance in B. tabaci.