PDF(Pubmed)
Abstract：
Transmission of many plant viruses relies on phloem-feeding insect vectors. However, how plant viruses directly modulate insect behavior is largely unknown. Barley yellow striate mosaic virus (BYSMV) is transmitted by the small brown planthopper (SBPH, Laodelphax striatellus). Here, we show that BYSMV infects the central nervous system (CNS) of SBPHs, induces insect hyperactivity, and prolongs phloem feeding duration. The BYSMV accessory protein P6 interacts with the COP9 signalosome subunit 5 (LsCSN5) of SBPHs and suppresses LsCSN5-regulated de-neddylation from the Cullin 1 (CUL1), hereby inhibiting CUL1-based E3 ligases-mediated degradation of the circadian clock protein Timeless (TIM). Thus, virus infection or knockdown of LsCSN5 compromises TIM oscillation and induces high insect locomotor activity for transmission. Additionally, expression of BYSMV P6 in the CNS of transgenic Drosophila melanogaster disturbs circadian rhythm and induces high locomotor activity. Together, our results suggest the molecular mechanisms whereby BYSMV modulates locomotor activity of insect vectors for transmission.
摘要：
许多植物病毒的传播依赖于以韧皮部为食的昆虫载体。然而,植物病毒如何直接调节昆虫的行为在很大程度上是未知的。大麦黄色条纹花叶病毒（BYSMV）由小褐飞虱传播（SBPH，Laodelphoxstriatellus）。这里,我们显示BYSMV感染SBPH的中枢神经系统（CNS），诱导昆虫多动症，并延长韧皮部摄食时间。BYSMV辅助蛋白P6与SBPH的COP9信号体亚基5（LsCSN5）相互作用，并抑制LsCSN5调节的Cullin1（CUL1）的去neddylation，由此抑制基于CUL1的E3连接酶介导的昼夜节律时钟蛋白Timeless（TIM）的降解。因此，LsCSN5的病毒感染或敲除会损害TIM振荡，并诱导高昆虫运动活性进行传播。此外,BYSMVP6在转基因果蝇中枢神经系统中的表达会扰乱昼夜节律并诱导高运动活性。一起,我们的结果提示了BYSMV调节昆虫载体的运动活性以进行传播的分子机制。
