BACKGROUND: Although the utility of double-stranded RNA (dsRNA)-mediated knockdown as an environmentally friendly pest management strategy has gained traction in recent years, its overall efficacy has been limited by poor stability and limited cellular uptake. Encapsulation of dsRNAs with various nanomaterials, however, has shown promise in overcoming these limitations. This study sought to investigate the biological efficacy of an oral dsRNA nanomaterial mixture targeting the CYP15C1 gene product in the economically important rice pest, Chilo suppressalis.RESULTS: A putative CYP15C1 ortholog was cloned from C. suppressalis midguts. The transcript is downregulated in fifth-instar larvae and is most highly expressed in heads. RNA interference (RNAi)-mediated knockdown of CsCYP15C1 was associated with significantly increased mortality. More importantly, feeding a dsRNA-nanomaterial mixture significantly increased larval mortality compared with feeding dsRNA alone.CONCLUSION: A critical role for CsCYP15C1 function in molting is supported by sequence similarity with known juvenile hormone epoxidases, its expression profile, and abnormal molting phenotypes associated with RNA-mediated knockdown. CsCYP15C1 is thus a prime target for controlling C. suppressalis. Furthermore, RNAi-mediated characterization of candidate gene function can be enhanced by incorporating an enveloping nanomaterial.

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The striped rice stem borer, Chilo suppressalis Walker, is one of the most destructive rice pests in Asia. Insecticidal crystal proteins (Cry toxins) produced by Bacillus thuringiensis are widely used as biopesticides or in developing transgenic crops for pest management. In this study, we tested the involvement of two newly cloned C. suppressalis cadherins (CsCAD3 and CsCAD4) in the toxicity of Cry1Ab/Ac, Cry2Aa and Cry1Ca. Our results showed that CsCAD4 was expressed highest in the midgut, whereas CsCAD3 was expressed highest in the epidermis. The feeding of double-stranded RNA specific to CsCAD3 and CsCAD4 respectively significantly suppressed the expressions of target gene. The knockdown of CsCAD3 significantly reduced the mortality of larvae to Cry1Ab/Ac, whereas knockdown of CsCAD4 significantly decreased the larval susceptibility to Cry2Aa. In contrast, reduced expressions of CsCAD3 or CsCAD4 were not interacted with larval susceptibility to Cry1Ca. Our results suggest that CsCAD3 and CsCAD4 function in Cry toxin toxicity and these findings will help us to better understand the action mechanism of Cry toxins in C. suppressalis.

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