The infection of host plants by many different viruses causes reactive oxygen species (ROS) accumulation and yellowing symptoms, but the mechanisms through which plant viruses counteract ROS-mediated immunity to facilitate infection and symptom development have not been fully elucidated. Most plant viruses are transmitted by insect vectors in the field, but the molecular mechanisms underlying virus‒host–insect interactions are unclear. In this study, we investigated the interactions among wheat, barley yellow dwarf virus (BYDV), and its aphid vector and found that the BYDV movement protein (MP) interacts with both wheat catalases (CATs) and the 26S proteasome ubiquitin receptor non-ATPase regulatory subunit 2 homolog (PSMD2) to facilitate the 26S proteasome-mediated degradation of CATs, promoting viral infection, disease symptom development, and aphid transmission. Overexpression of the BYDV gene in wheat enhanced the degradation of CATs, which leading to increased accumulation of ROS and thereby enhanced viral infection. Interestingly, transgenic wheat lines overexpressing BYDV showed significantly reduced proliferation of wingless aphids and an increased number of winged aphids. Consistent with this observation, silencing of genes also enhanced viral accumulation and reduced the proliferation of wingless aphids but increased the occurrence of winged aphids. In contrast, transgenic wheat plants overexpressing exhibited the opposite changes and showed increases in grain size and weight upon infection with BYDV. Biochemical assays demonstrated that BYDV MP interacts with PSMD2 and promotes 26S proteasome-mediated degradation of TaCAT1 likely in a ubiquitination-independent manner. Collectively, our study reveals a molecular mechanism by which a plant virus manipulates the ROS production system of host plants to facilitate viral infection and transmission, shedding new light on the sophisticated interactions among viruses, host plants, and insect vectors.

中文翻译：

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一种病毒运动蛋白以宿主过氧化氢酶为目标，进行 26S 蛋白酶体介导的降解，以促进小麦中的病毒感染和蚜虫传播

许多不同病毒对宿主植物的感染会导致活性氧（ROS）积累和黄化症状，但植物病毒抵消ROS介导的免疫以促进感染和症状发展的机制尚未完全阐明。大多数植物病毒在田间通过昆虫媒介传播，但病毒-宿主-昆虫相互作用的分子机制尚不清楚。在这项研究中，我们研究了小麦、大麦黄矮病毒（BYDV）及其蚜虫载体之间的相互作用，发现BYDV运动蛋白（MP）与小麦过氧化氢酶（CAT）和26S蛋白酶体泛素受体非ATP酶相互作用调节亚基 2 同源物 (PSMD2) 可促进 26S 蛋白酶体介导的 CAT 降解，促进病毒感染、疾病症状发展和蚜虫传播。小麦中 BYDV 基因的过度表达增强了 CAT 的降解，从而导致 ROS 积累增加，从而增强病毒感染。有趣的是，过表达 BYDV 的转基因小麦品系显示无翅蚜虫的增殖显着减少，而有翅蚜虫的数量增加。与这一观察结果一致，基因沉默也增强了病毒积累并减少了无翅蚜虫的增殖，但增加了有翅蚜虫的发生。相反，过度表达的转基因小麦植株表现出相反的变化，并在感染 BYDV 后表现出籽粒大小和重量增加。生化检测表明，BYDV MP 与 PSMD2 相互作用，并可能以不依赖泛素化的方式促进 26S 蛋白酶体介导的 TaCAT1 降解。总的来说，我们的研究揭示了植物病毒操纵宿主植物的活性氧产生系统以促进病毒感染和传播的分子机制，为病毒、宿主植物和昆虫媒介之间复杂的相互作用提供了新的线索。