State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
State Key Laboratory of Rice Biology, Institute of Biotechnology, Zhejiang University, Hangzhou, 310029, China.
Sci China Life Sci. 2024 Jan;67(1):161-174. doi: 10.1007/s11427-022-2377-1. Epub 2023 Oct 12.
N-methyladenosine (mA) is the most abundant eukaryotic mRNA modification and is involved in various biological processes. Increasing evidence has implicated that mA modification is an important anti-viral defense mechanism in mammals and plants, but it is largely unknown how mA regulates viral infection in plants. Here we report the dynamic changes and functional anatomy of mA in Nicotiana benthamiana and Solanum lycopersicum during Pepino mosaic virus (PepMV) infection. mA modification in the PepMV RNA genome is conserved in these two species. Overexpression of the mA writers, mRNA adenosine methylase A (MTA), and HAKAI inhibit the PepMV RNA accumulation accompanied by increased viral mA modifications, whereas deficiency of these writers decreases the viral RNA mA levels but enhances virus infection. Further study reveals that the cytoplasmic YTH-domain family protein NbECT2A/2B/2C as mA readers are involved in anti-viral immunity. Protein-protein interactions indicate that NbECT2A/2B/2C interact with nonsense-mediated mRNA decay (NMD)-related proteins, including NbUPF3 and NbSMG7, but not with NbUPF1. mA modification-mediated restriction to PepMV infection is dependent on NMD-related factors. These findings provide new insights into the functionality of mA anti-viral activity and reveal a distinct immune response that NMD factors recognize the mA readers-viral mA RNA complex for viral RNA degradation to limit virus infection in plants.
N6-甲基腺苷（m6A）是最丰富的真核 mRNA 修饰，参与多种生物学过程。越来越多的证据表明，m6A 修饰是哺乳动物和植物中重要的抗病毒防御机制，但 m6A 如何调节植物中的病毒感染在很大程度上尚不清楚。在这里，我们报告了在 Pepino 花叶病毒（PepMV）感染过程中 Nicotiana benthamiana 和 Solanum lycopersicum 中 m6A 的动态变化和功能解剖。这两个物种的 PepMV RNA 基因组中的 m6A 修饰是保守的。mA 书写器，mRNA 腺苷甲基转移酶 A（MTA）和 HAKAI 的过表达抑制 PepMV RNA 的积累，同时增加病毒 m6A 修饰，而这些书写器的缺乏则降低病毒 RNA m6A 水平，但增强病毒感染。进一步的研究表明，细胞质 YTH 结构域家族蛋白 NbECT2A/2B/2C 作为 m6A 阅读器参与抗病毒免疫。蛋白-蛋白相互作用表明，NbECT2A/2B/2C 与无意义介导的 mRNA 降解（NMD）相关蛋白相互作用，包括 NbUPF3 和 NbSMG7，但不与 NbUPF1 相互作用。依赖于 m6A 修饰的 PepMV 感染限制依赖于 NMD 相关因子。这些发现为 m6A 抗病毒活性的功能提供了新的见解，并揭示了一种独特的免疫反应，即 NMD 因子识别 mA 阅读器-病毒 m6A RNA 复合物，用于病毒 RNA 降解，以限制植物中的病毒感染。
