Nature Communications | 中国农大王献兵团队揭示植物弹状病毒BYSMV调节昆虫介体的运动活性以增强病毒传播

以下文章来源于植物胁迫与抗逆研究 ，作者吴昕扬

近日，由中国农大王献兵团队在Nature Communications发表了题为《A plant cytorhabdovirus modulates locomotor activity of insect vectors to enhance virus transmission》的研究论文，揭示了植物弹状病毒BYSMV调节昆虫介体的运动活性以增强病毒传播。

许多植物病毒的传播依赖于以韧皮部为食的昆虫媒介。然而，在某种程度上而言，植物病毒如何直接调节昆虫行为仍然是未知的。大麦黄条纹花叶病毒（BYSMV）由灰飞虱（SBPH）传播。

在本研究中，作者发现BYSMV感染SBPH的中枢神经系统（CNS），诱导昆虫多动，并延长韧皮部进食时间。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调节的来自Cullin 1（CUL1）的去甲酰化，从而抑制基于CUL1的E3连接酶介导的对昼夜节律时钟蛋白TIM的降解。

因此，病毒感染或LsCSN5的敲除损害了TIM振荡，并诱导了昆虫传播运动活性提高。此外，BYSMV P6在转基因果蝇中枢神经系统中的表达也扰乱昼夜节律并诱导高运动活性。

总之，本研究的结果表明了BYSMV调节昆虫媒介传播运动活性的分子机制。

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.

本文转载自植物胁迫与抗逆研究

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