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<p>N<sup>6</sup>-methyladenosine (m<sup>6</sup>A), the most prevalent internal mRNA modification, regulates plant development and stress responses through modulating various mRNA metabolic processes and epigenetic effects. Although well studied in animals, its roles in plant–virus interactions have only recently begun to be elucidated. Multiple plant viruses carry m<sup>6</sup>A modifications on their RNAs, validated by MeRIP-seq, LC–MS/MS, and direct RNA sequencing. Viral RNAs acquire m<sup>6</sup>A through the recruitment or relocalization of host methyltransferase complexes, which is often mediated by viral proteins. Functionally, m<sup>6</sup>A can restrict infection by promoting viral RNA decay via YTH-domain readers and RNA surveillance pathways, or alternatively stabilize viral RNAs to enhance replication and systemic spread. In turn, viruses disrupt the functionality of host m<sup>6</sup>A machinery to promote infection. Moreover, viral infection reprograms host m<sup>6</sup>A homeostasis, altering methylation landscapes in immune and hormone pathways. These findings establish m<sup>6</sup>A as a dynamic epitranscriptomic switch in plant-virus interactions, with promising implications for antiviral strategies and crop improvement.</p>

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The expanding role of m6A RNA modification in plant-virus dynamics: friend, foe, or both?

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月6日

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  • Jia-Hui Liu,
  • Hao Yu,
  • Cheng-Guo Duan

摘要

N6-methyladenosine (m6A), the most prevalent internal mRNA modification, regulates plant development and stress responses through modulating various mRNA metabolic processes and epigenetic effects. Although well studied in animals, its roles in plant–virus interactions have only recently begun to be elucidated. Multiple plant viruses carry m6A modifications on their RNAs, validated by MeRIP-seq, LC–MS/MS, and direct RNA sequencing. Viral RNAs acquire m6A through the recruitment or relocalization of host methyltransferase complexes, which is often mediated by viral proteins. Functionally, m6A can restrict infection by promoting viral RNA decay via YTH-domain readers and RNA surveillance pathways, or alternatively stabilize viral RNAs to enhance replication and systemic spread. In turn, viruses disrupt the functionality of host m6A machinery to promote infection. Moreover, viral infection reprograms host m6A homeostasis, altering methylation landscapes in immune and hormone pathways. These findings establish m6A as a dynamic epitranscriptomic switch in plant-virus interactions, with promising implications for antiviral strategies and crop improvement.