He Rongrong, Li Yinzi, Bernards Mark A, Wang Aiming
London Research and Development Centre, Agriculture and Agri-Food Canada, London, ON, N5V 4T3, Canada.
Department of Biology, Western University, 1151 Richmond St., London, ON, N6A 5B7, Canada.
New Phytol. 2025 Jan;245(1):299-317. doi: 10.1111/nph.20233. Epub 2024 Nov 12.
Pathogenesis-related (PR) proteins are induced by abiotic and biotic stresses and generally considered as part of the plant defense mechanism. However, it remains yet largely unclear if and how they are involved in virus infection. Our recent quantitative, comparative proteomic study identified three PR-5 family proteins that are significantly differentially accumulated in the plasmodesmata (PD)-enriched fraction isolated from Nicotiana benthamiana leaves infected by turnip mosaic virus (TuMV). In this study, we employed the TuMV-Arabidopsis pathosystem to characterize the involvement of two Arabidopsis orthologs, AtOSM34 and AtOLP of the three N. benthamiana PR-5-like proteins. We show that AtOSM34 and AtOLP are PD-localized proteins and their expression is up- and downregulated in response to TuMV infection, respectively. Deficiency or overexpression of AtOLP does not affect viral RNA accumulation. Knockdown of AtOSM34 inhibits TuMV infection, whereas its overexpression promotes viral infection. We further demonstrate that AtOSM34 functions as a proviral factor through diminishing PD callose deposition to promote viral intercellular movement, targeting the viral replication complex to enhance viral replication, and suppressing the ROS-mediated antiviral response. Taken together, these data suggest that TuMV has evolved the ability to selectively upregulate and subvert AtOSM34, a PR-5 family protein to assist its infection.
病程相关（PR）蛋白由非生物和生物胁迫诱导产生，通常被认为是植物防御机制的一部分。然而，它们是否以及如何参与病毒感染在很大程度上仍不清楚。我们最近的定量比较蛋白质组学研究鉴定出三种PR-5家族蛋白，它们在从感染芜菁花叶病毒（TuMV）的本氏烟草叶片中分离出的富含胞间连丝（PD）的组分中显著差异积累。在本研究中，我们利用TuMV-拟南芥病理系统来表征三种本氏烟草PR-5样蛋白的两个拟南芥直系同源物AtOSM34和AtOLP的参与情况。我们表明AtOSM34和AtOLP是定位于PD的蛋白，它们的表达分别在TuMV感染时上调和下调。AtOLP的缺失或过表达不影响病毒RNA积累。AtOSM34的敲低抑制TuMV感染，而其过表达促进病毒感染。我们进一步证明，AtOSM34通过减少PD胼胝质沉积以促进病毒细胞间移动、将病毒复制复合体靶向以增强病毒复制以及抑制ROS介导的抗病毒反应，作为一种病毒促进因子发挥作用。综上所述，这些数据表明TuMV已经进化出选择性上调和颠覆PR-5家族蛋白AtOSM34以协助其感染的能力。
