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.
Subject(s)
Hemiptera , Insecticides , MicroRNAs , Animals , Insecticides/pharmacology , Insecticides/metabolism , Pyrazoles/metabolism , Hemiptera/metabolism , Cytochrome P-450 Enzyme System/metabolism , MicroRNAs/genetics , MicroRNAs/metabolismABSTRACT
BACKGROUND: Tomato chlorosis virus (ToCV) is associated with tomato yellow leaf disorder diseases in more than 20 countries. ToCV can be transmitted in a semipersistent manner by whitefly vectors such as Bemisia tabaci. Controlling the vector pests by using chemical insecticides is an efficient and effective approach to reduce and interrupt the virus transmission. Pyrifluquinazon is a new pyridine azomethine derivative, showing insecticidal toxicity to sucking pests by disturbing their feeding behavior. However, limited attention has been paid to the performance of pyrifluquinazon against B. tabaci and ToCV transmission. RESULT: This study showed the lethal concentration of 50% (LC50 ) values of pyrifluquinazon to 22 B. tabaci field populations ranged from 0.54 to 2.44 mg L-1 , and the baseline susceptibility of B. tabaci to pyrifluquinazon was 1.24 mg L-1 with a 95% confidence limit of 0.35-1.85 mg L-1 . Pyrifluquinazon and afidopyropen did not show cross-resistance to dinotefuran and pymetrozine in B. tabaci, which both inhibited the feeding activities of B. tabaci. The antifeedant concentration of 50% (AFC50 ) values at 48 h were 0.70 mg L-1 for pyrifluquinazon and 2.13 mg L-1 for afidopyropen. Foliar application of pyrifluquinazon and afidopyropen reduced the ToCV transmission by 40.91% and 33.33%, respectively and significantly decreased the ToCV loads in tomato plants under laboratory conditions. CONCLUSION: These results provided new information about the effects of modulators of the vanilloid-type transient receptor potential channel on the toxicity to B. tabaci and inhibition of ToCV transmission. © 2023 Society of Chemical Industry.
Subject(s)
Hemiptera , Solanum lycopersicum , Animals , Feeding Behavior , Hemiptera/physiologyABSTRACT
Bemisia tabaci is an important agricultural sucking pest, and it develops serious resistance to various insecticides. Although cytochrome P450 was involved in the resistance to cyantraniliprole, limited studies have been conducted on B. tabaci. In the present study, piperonyl butoxide significantly increased the toxicity of cyantraniliprole. P450 activities in two resistant populations were 1.97- and 2.17-fold higher than that in the susceptible population. Among 79 P450 genes, CYP6CX3 expressions in two resistant populations were 3.08- and 3.67-fold higher than that in the susceptible population. When CYP6CX3 was knocked down, the toxicity of cyantraniliprole increased significantly. The LC50 value of cyantraniliprole to the Drosophila melanogaster line overexpressing B. tabaci CYP6CX3 increased 7.34-fold. The content of cyantraniliprole was decreased by 25.74 ± 4.27% after mixing with CYP6CX3 and CPR for 2 h. These results suggested that the overexpression of CYP6CX3 was likely involved in the resistance to cyantraniliprole in B. tabaci.
