Potyviruses recruit host eIF4A3 to block m6A-mediated RNA decay by steric hindrance of viral RNA methylation in plants

作者：Dezhi Peng, Laihua Dong, Pei Wang, Lianyi Zang, Jinhao Xie, Hao Wang, X. Li, Fan ZaiFeng, Tao Zhou, Kaitong Du · 发表于：Nucleic Acids Research · 年份：2026 · DOI：10.1093/nar/gkaf1432 · 被引用次数：2 · 研究领域：RNA modifications and cancer、Plant Virus Research Studies、Bacteriophages and microbial interactions

N 6-methyladenosine (m6A), a critical epitranscriptomic modification, regulates RNA metabolism and antiviral defenses. However, how pathogens evade m6A-mediated RNA decay in plants remains poorly understood. Here, we uncover a dynamic m6A modification arms race during infection of sugarcane mosaic virus (SCMV), a prevalent potyvirus that infects maize and causes 20%-80% yield loss. We demonstrate that maize m6A methyltransferase (ZmMTA) specifically deposits m6A at A6556 of the SCMV genomic RNA, enabling recognition by the m6A reader EVOLUTIONARILY CONSERVED C-TERMINAL REGION 23 (ZmECT23). ZmECT23 directly recruits the ZmCCR4-NOT (carbon catabolite repressor 4-negative on TATA) complex to facilitate viral RNA decay. Strikingly, SCMV counters the defense via its nuclear inclusion protein a protease (NIa-Pro), which hijacks maize eukaryotic initiation factor 4A-III (ZmeIF4A3) into viral replication complexes. ZmeIF4A3 sterically blocks ZmMTA-mediated m6A deposition, thereby preventing viral RNA from degradation. Mechanistic conservation is observed in potato virus Y and turnip mosaic virus, two other potyviruses that are modified with m6A. Our study identifies eIF4A3 as a key m6A regulator in plants and reveals a strategy used by potyviruses to subvert m6A-based immunity via exploiting host RNA helicases. These findings provide mechanistic insights into host-pathogen interactions as mediated by m6A and suggest eIF4A3 as a potential target for engineering m6A-based antiviral cro...