Abstract
No evidence has shown whether insect-borne viruses manipulate the c-Jun N-terminal kinase (JNK) signaling pathway of vector insects. Using a system comprising the plant virus Rice stripe virus (RSV) and its vector insect, the small brown planthopper, we have studied the response of the vector insect's JNK pathway to plant virus infection. We found that RSV increased the level of Tumor Necrosis Factor-α and decreased the level of G protein Pathway Suppressor 2 (GPS2) in the insect vector. The virus capsid protein competitively bound GPS2 to release it from inhibiting the JNK activation machinery. We confirmed that JNK activation promoted RSV replication in the vector, whereas JNK inhibition caused a significant reduction in virus production and thus delayed the disease incidence of plants. These findings suggest that inhibition of insect vector JNK may be a useful strategy for controling the transmission of plant viruses.
Highlights
Most plant viruses depend on sap-feeding insects from the order Hemiptera for their transmission (Hogenhout et al, 2008)
Our study clarifies for the first time that the virus enhances its replication in a vector insect by activating the vector’s Jun N-terminal kinase (JNK) pathway, and thatJNK inhibition results in a delayed disease incidence in plants
We provide a model to summarize how Rice stripe virus (RSV) manipulates the upstream signal molecules and the downstream suppressor to activate the JNK pathway in the planthoppers (Figure 7)
Summary
Most plant viruses depend on sap-feeding insects from the order Hemiptera for their transmission (Hogenhout et al, 2008). The success and efficiency of virus transmission, especially for the persistent-propagative viruses, depend on specific interactions between the virus and proteins of the vector insects, allowing transport of the virus in and out of insect tissues and overcoming insect immune reactions for successful replication (Blanc et al, 2014). As with most persistent-propagative viruses, RSV cannot be transmitted directly between plants in the field, and there is a large difference in pathogenicity of the virus from the insect vectors and from the viruliferous plants (Zhao et al, 2016b). CP is the most abundant viral protein and plays a crucial role in the retention and movement of the virus in the insect vector (Blanc et al, 2014)
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