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Proteins of the alkylation B (AlkB) superfamily show RNA demethylase activity removing methyl adducts from N6‐methyladenosine (m6A). m6A is a reversible epigenetic mark of RNA that regulates human virus replication but has unclear roles in plant virus infection. We focused on Potyvirus—the largest genus of plant RNA viruses—and report here the identification of AlkB domains within P1 of endive necrotic mosaic virus (ENMV) and an additional virus of a putative novel species within Potyvirus. We show that Nicotiana benthamiana m6A levels are reduced by infection of plum pox virus (PPV) and potato virus Y (PVY). The two potyviruses lack AlkB and the results suggest a general involvement of RNA methylation in potyvirus infection and evolution. Methylated RNA immunoprecipitation sequencing of virus‐infected samples showed that m6A peaks are enriched in plant transcript 3′ untranslated regions and in discrete internal and 3′ terminal regions of PPV and PVY genomes. Down‐regulation of N. benthamiana AlkB homologues of the plant‐specific ALKBH9 clade caused a significant decrease in PPV and PVY accumulation. In summary, our study provides evolutionary and experimental evidence that supports the m6A implication and the proviral roles of AlkB homologues in Potyvirus infection. [ABSTRACT FROM AUTHOR]

Simple Summary: N6-methyladenosine (m6A) is the most prevalent modification in the mRNAs of many eukaryotic species. The abundance and effects of m6A are determined by dynamic interactions between its methyltransferases ("writers"), demethylases ("erasers"), and binding proteins ("readers"). It has been indicated that there is a strong correlation between m6A and virus infection in mammals. In the case of plant virus infection, it appears that m6A plays a dual role. On the one hand, m6A acts as a plant immune response induced by virus infection, inhibiting viral replication or translation through methylation of viral genome RNAs. On the other hand, m6A acts as part of an infection strategy employed by plant viruses to overcome the host immune system by interacting with m6A-related proteins. We proposed that antagonists of m6A-related proteins might be used to design new strategies for plant virus control in the future. In recent years, m6A RNA methylation has attracted broad interest and is becoming a hot research topic. It has been demonstrated that there is a strong association between m6A and viral infection in the human system. The life cycles of plant RNA viruses are often coordinated with the mechanisms of their RNA modification. Here, we reviewed recent advances in m6A methylation in plant viruses. It appears that m6A methylation plays a dual role during viral infection in plants. On the one hand, m6A methylation acts as an antiviral immune response induced by virus infection, which inhibits viral replication or translation through the methylation of viral genome RNAs. On the other hand, plant viruses could disrupt the m6A methylation through interacting with the key proteins of the m6A pathway to avoid modification. Those plant viruses containing ALKB domain are discussed as well. Based on this mechanism, we propose that new strategies for plant virus control could be designed with competitive antagonists of m6A-associated proteins. [ABSTRACT FROM AUTHOR]