Background
Migratory insect infestation caused by
Sogatella furcifera
is a serious threat to rice production. The most effective method available for
S. furcifera
control is intensive insecticide spraying, which cause widespread resistance. RNA interference (RNAi) insecticides hold enormous potential in managing pest resistance. However, the instability and the poor efficiency of cross-kingdom RNA trafficking are key obstacles for the application in agricultural pest management.
Methods
We present dendritic mesoporous silica nanoparticles (DMSNs)-based nanocarrier for delivering siRNA and nitenpyram to inhibit the metabolic detoxification and development of
S. furcifera
, thereby preventing its proliferation.
Results
This nano complex (denoted as N@UK-siRNA/DMSNs) significantly enhanced the stability of siRNA (efficacy lasting 21 days) and released cargos in GSH or planthopper bodily fluid with a maximum release rate of 84.99%. Moreover, the released UK-siRNA targeting two transcription factors (
Ultraspiracle
and
Krüppel-homolog 1
) downregulated the developmental genes
Ultraspiracle
(0.09-fold) and
Krüppel-homolog 1
(0.284-fold), and downstream detoxification genes ABC
SfABCH4
(0.016-fold) and P450
CYP6FJ3
(0.367-fold).
Conclusion
The N@UK-siRNA/DMSNs inhibited pest development and detoxification, significantly enhancing susceptibility to nitenpyram to nanogram level (LC
50
is 250–252 ng/mL), resulting in a 5.37–7.13-fold synergistic ratio. This work proposes a comprehensive management strategy for controlling
S. furcifera
to ensure the green and safe production of rice.
Graphical Abstract
Schematic fabrication of the N@UK-siRNA/DMSNs and the molecular mechanism resolution of improving the sensitivity of
S. furcifera
to nitenpyram. The nitenpyram and UK-siRNA are assembled onto the DMSNs by interfacial modification. With phloem and xylem pathway, the N@UK-siRNA/DMSNs could transport bi-directionally to the feeding sites of
S. furcifera
and then release nitenpyram and UK-siRNA in
S. furcifera
in response to glutathione (GSH). The UK-siRNA released from N@UK-siRNA/DMSNs would downregulate the developmental genes U
SP
and
Kr-H1
. The releasing nitenpyram would competitively bind to acetylcholine (ACh) receptors, inhibiting the transmission of nerve impulses
Supplementary Information
The online version contains supplementary material available at 10.1186/s12951-024-02966-8.