Wang Wei, Zhao Wan, Li Jing, Luo Lan, Kang Le, Cui Feng
State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
University of Chinese Academy of Sciences, Beijing, China.
Elife. 2017 Jul 18;6:e26591. doi: 10.7554/eLife.26591.
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 (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.
尚无证据表明虫媒病毒是否会操纵媒介昆虫的c-Jun氨基末端激酶（JNK）信号通路。我们利用包含植物病毒（水稻条纹病毒，RSV）及其媒介昆虫灰飞虱的系统，研究了媒介昆虫JNK通路对植物病毒感染的反应。我们发现，RSV提高了昆虫媒介中肿瘤坏死因子-α的水平，并降低了G蛋白通路抑制因子2（GPS2）的水平。病毒衣壳蛋白竞争性结合GPS2，使其从抑制JNK激活机制中释放出来。我们证实，JNK激活促进了RSV在媒介中的复制，而抑制JNK则导致病毒产量显著降低，从而延缓了植物疾病的发生。这些发现表明，抑制昆虫媒介的JNK可能是控制植物病毒传播的一种有效策略。
