2017年7月18日，国际知名期刊《eLife》杂志在线发表了中国科学院动物研究所崔峰研究团队题为“The c-Jun N-terminal kinase pathway of a vector insect is activated by virus capsid protein and promotes viral replication”的研究论文，研究在RSV与介体昆虫相互作用研究方面取得了新进展。本研究由崔峰研究员与康乐研究员共同完成，崔峰及康乐为共同通讯作者，博士后王炜、助理研究员赵婉以及博士生李京为共同第一作者。

水稻条纹病毒(RSV)是一种虫媒纤细属病毒，主要由介体昆虫灰飞虱以持久、增殖型方式传播，导致东南亚水稻等农作物严重减产。该发现RSV的衣壳蛋白CP竞争性结合灰飞虱的G蛋白通路抑制因子II(GPS2)，减弱了GPS2对jnk激活复合物的抑制作用，从而提高了JNK的磷酸化水平。同时，病毒还提高了JNK信号通路上游的Tumor Necrosis Factor-α的表达，降低了GPS2的表达。JNK磷酸化水平的提高增加了RSV在昆虫体内的增殖，而通过干扰JNK基因的表达或使用JNK激活的抑制剂，RSV在昆虫体内的增殖会受到抑制，并延缓植物的发病。这一研究结果揭示了JNK信号通路在病毒复制过程中的关键作用，为今后控制RSV的传播提供了新思路。

崔峰研究团队长期从事介体昆虫-病毒-植物分子互作的研究，致力于揭示介体昆虫在病毒传播过程中的关键作用，在该领域以通讯作者在New Phytol, FASEB J, Curr Issues Mol Biol, BMC genomics, Insect Biochem Mol Biol等多个重要学术期刊上发表了一系列相关成果。

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.