SUMOylated viral polymerase reprograms host epitranscriptome to promote infection in plants

N6-methyladenosine (m ⁶ A), as the most abundant internal RNA modification, plays crucial, dynamic roles in in plant biology. By regulating gene expression at the post-transcriptional level, m ⁶ A modification has a broad impact on plant growth and development, and environmental stress responses including pathogen defense response. Here, we report that turnip mosaic virus (TuMV, Potyvirus rapae ) actively reprograms the global host m ⁶ A landscapes to promote infection in Arabidopsis thaliana and Nicotiana benthamiana . We show that TuMV infection induces extensive genome-wide m ⁶ A hypomethylation, suppressing more than 60% of conserved m ⁶ A modified RNAs. This is accompanied by compromised abundance and translational efficiency of defense-associated transcripts that are normally promoted by m ⁶ A modification. We further present evidence that the SUMOylated form of the TuMV RNA-dependent RNA polymerase NIb physically disrupts the m ⁶ A writer complex by displacing its core component MTB (methyltransferase B) and sequestering another key subunit MTA (mRNA adenosine methylase) in cytoplasmic viral replication factories, thereby suppressing m ⁶ A deposition. Expression of SUMOylated NIb alone is sufficient to manipulate global m ⁶ A modification and transcriptome reprogramming in the absence of viral infection. These findings reveal that viral RNA polymerase deploys a SUMO-mediated ‘writer hijacking’ strategy to remodel the host epigenetic transcriptome, thereby constructing an intracellular niche favorable for viral survival and replication.