PEBP balances apoptosis and autophagy in whitefly upon arbovirus infection
Shifan Wang, Huijuan Guo, Keyan Zhu-Salzman, Feng Ge & Yucheng Sun
山东省农业科学院植物保护研究所研究员戈峰与中科院动物研究所农业虫害鼠害综合治理研究国家重点实验室研究员孙玉诚及其团队合作，首次发现磷脂酰乙醇胺结合蛋白（PEBP4）是调节获毒烟粉虱胞内免疫稳态的关键分子，通过维持其细胞凋亡与自噬作用相互拮抗的中度免疫平衡，以达到高效传毒的新机制。相关论文2月11日发表于《自然—通讯》。
文章指出，烟粉虱是全球分布的“超级害虫”，由它专性传播的的植物病害番茄黄化曲叶病毒（TYLCV）每年造成农作物上百亿元的损失，尤其是对番茄等蔬菜生产构成了极大威胁。但烟粉虱如何调节和维持其体内胞内细胞凋亡与自噬作用的免疫稳态，以使烟粉虱及其携带的病毒长期共存并高效传毒的机制一直不清楚，该文为其机制探究提出了新的切入点，为防控虫媒病毒传播提供了理论依据。
众所周知，细胞免疫稳态如何被维持和调节是Science 发布认定的“最前沿的125个科学问题”之一。该研究通过大量的试验发现，TYLCV 病毒衣壳蛋白在烟粉虱中肠和唾液腺细胞的质膜上通过“劫持”PEBP4，同步激活细胞凋亡与自噬作用，二者之间的相互拮抗形成了中度免疫平衡。过高的免疫激发不利于烟粉虱持毒，而过低的免疫响应致使烟粉虱携带病毒量过高，其适合度代偿过大，不利于生存。显然，只有PEBP4维持适度的免疫平衡，才能保障烟粉虱高效传毒，奠定了其与虫媒病毒长期共存的本质。
该研究首次阐明了烟粉虱传播TYLCV的胞内免疫基础，揭示了烟粉虱通过平衡其细胞凋亡与自噬作用的免疫稳态分子机制，极大推动了媒介昆虫免疫耐受研究的发展。这不但在媒介生物学领域创新具有重要的理论意义，而且为控制“世界头号害虫”烟粉虱传播病毒、保护蔬菜生产安全提供了新思路，有重大的应用前景。
来源：中国科学报 王方
Abstract
Apoptosis and autophagy are two common forms of programmed cell death (PCD) used by host organisms to fight against virus infection. PCD in arthropod vectors can be manipulated by arboviruses, leading to arbovirus-vector coexistence, although the underlying mechanism is largely unknown. In this study, we find that coat protein (CP) of an insect-borne plant virus TYLCV directly interacts with a phosphatidylethanolamine-binding protein (PEBP) in its vector whitefly to downregulate MAPK signaling cascade. As a result, apoptosis is activated in the whitefly increasing viral load. Simultaneously, the PEBP4-CP interaction releases ATG8, a hallmark of autophagy initiation, which reduces arbovirus levels. Furthermore, apoptosis-promoted virus amplification is prevented by agonist-induced autophagy, whereas the autophagy-suppressed virus load is unaffected by manipulating apoptosis, suggesting that the viral load is predominantly determined by autophagy rather than by apoptosis. Our results demonstrate that a mild intracellular immune response including balanced apoptosis and autophagy might facilitate arbovirus preservation within its whitefly insect vector.
