m 6 A modification plays an integral role in mRNA stability and translation during pattern-triggered immunity.

Plants employ distinct mechanisms to respond to environmental changes. Modification of mRNA by N  6 -methyladenosine (m 6 A), known to affect the fate of mRNA, may be one such mechanism to reprogram mRNA processing and translatability upon stress. However, it is difficult to distinguish a direct role from a pleiotropic effect for this modification due to its prevalence in RNA. Through characterization of the transient knockdown-mutants of m 6 A writer components and mutants of specific m 6 A readers, we demonstrate the essential role that m 6 A plays in basal resistance and pattern-triggered immunity (PTI). A global m 6 A profiling of mock and PTI-induced Arabidopsis plants as well as formaldehyde fixation and cross-linking immunoprecipitation-sequencing of the m 6 A reader, EVOLUTIONARILY CONSERVED C-TERMINAL REGION2 (ECT2) showed that while dynamic changes in m 6 A modification and binding by ECT2 were detected upon PTI induction, most of the m 6 A sites and their association with ECT2 remained static. Interestingly, RNA degradation assay identified a dual role of m 6 A in stabilizing the overall transcriptome while facilitating rapid turnover of immune-induced mRNAs during PTI. Moreover, polysome profiling showed that m 6 A enhances immune-associated translation by binding to the ECT2/3/4 readers. We propose that m 6 A plays a positive role in plant immunity by destabilizing defense mRNAs while enhancing their translation efficiency to create a transient surge in the production of defense proteins.