2017年7月18日，國際知名期刊《eLife》雜志在線(xiàn)發(fā)表了中國科學(xué)院動(dòng)物研究所崔峰研究團隊題為“The c-Jun N-terminal kinase pathway of a vector insect is activated by virus capsid protein and promotes viral replication”的研究論文，研究在RSV與介體昆蟲(chóng)相互作用研究方面取得了新進(jìn)展。本研究由崔峰研究員與康樂(lè )研究員共同完成，崔峰及康樂(lè )為共同通訊作者，博士后王煒、助理研究員趙婉以及博士生李京為共同第一作者。

水稻條紋病毒(RSV)是一種蟲(chóng)媒纖細屬病毒，主要由介體昆蟲(chóng)灰飛虱以持久、增殖型方式傳播，導致東南亞水稻等農作物嚴重減產(chǎn)。該發(fā)現RSV的衣殼蛋白CP競爭性結合灰飛虱的G蛋白通路抑制因子II(GPS2)，減弱了GPS2對jnk激活復合物的抑制作用，從而提高了JNK的磷酸化水平。同時(shí)，病毒還提高了JNK信號通路上游的Tumor Necrosis Factor-α的表達，降低了GPS2的表達。JNK磷酸化水平的提高增加了RSV在昆蟲(chóng)體內的增殖，而通過(guò)干擾JNK基因的表達或使用JNK激活的抑制劑，RSV在昆蟲(chóng)體內的增殖會(huì )受到抑制，并延緩植物的發(fā)病。這一研究結果揭示了JNK信號通路在病毒復制過(guò)程中的關(guān)鍵作用，為今后控制RSV的傳播提供了新思路。

崔峰研究團隊長(cháng)期從事介體昆蟲(chóng)-病毒-植物分子互作的研究，致力于揭示介體昆蟲(chóng)在病毒傳播過(guò)程中的關(guān)鍵作用，在該領(lǐng)域以通訊作者在New Phytol, FASEB J, Curr Issues Mol Biol, BMC genomics, Insect Biochem Mol Biol等多個(gè)重要學(xué)術(shù)期刊上發(fā)表了一系列相關(guān)成果。

The c-Jun N-terminal kinase pathway of a vector insect is activated by virus capsid protein and promotes viral replication

原文摘要：

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.