Cyantraniliprole is the first diamide insecticide to have cross-spectrum activity against a broad range of insect orders. The insecticide, like other diamides, selectively acts on ryanodine receptor, destroys Ca2+ homeostasis, and ultimately causes insect death. Although expression regulations of genes associated with calcium signaling pathways are known to be involved in the response to diamides, little is known regarding the function of calmodulin (CaM), a typical Ca2+ sensor central in regulating Ca2+ homeostasis, in the stress response of insects to the insecticide. In this study, we cloned and identified the full-length complementary DNA of CaM in the whitefly, Bemisia tabaci (Gennadius), named BtCaM. Quantitative real-time reverse transcription polymerase chain reaction-based analyses showed that the messenger RNA level of BtCaM was rapidly induced from 1.51- to 2.43-fold by cyantraniliprole during 24 h. Knockdown of BtCaM by RNA interference increased the toxicity of cyantraniliprole in whiteflies by 42.85%. In contrast, BtCaM expression in Sf9 cells significantly increased the cells' tolerance to cyantraniliprole as much as 2.91-fold. In addition, the expression of BtCaM in Sf9 cells suppressed the rapid increase of intracellular Ca2+ after exposure to cyantraniliprole, and the maximum amplitude in the Sf9-BtCaM cells was only 34.9% of that in control cells (Sf9-PIZ/V5). These results demonstrate that overexpression of BtCaM is involved in the stress response of B. tabaci to cyantraniliprole through regulation of Ca2+ concentration. As CaM is one of the most evolutionarily conserved Ca2+ sensors in insects, outcomes of this study may provide the first details of a universal insect response to diamide insecticides.
Keywords: Bemisia tabaci; Ca2+ homeostasis; calmodulin; cyantraniliprole; insecticide stress; overexpression.
© 2020 Institute of Zoology, Chinese Academy of Sciences.