mA 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 -methyladenosine (mA), 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 mA writer components and mutants of specific mA readers, we demonstrate the essential role that mA plays in basal resistance and pattern-triggered immunity (PTI). A global mA profiling of mock and PTI-induced plants as well as formaldehyde fixation and cross-linking immunoprecipitation-sequencing of the mA reader, EVOLUTIONARILY CONSERVED C-TERMINAL REGION2 (ECT2) showed that while dynamic changes in mA modification and binding by ECT2 were detected upon PTI induction, most of the mA sites and their association with ECT2 remained static. Interestingly, RNA degradation assay identified a dual role of mA in stabilizing the overall transcriptome while facilitating rapid turnover of immune-induced mRNAs during PTI. Moreover, polysome profiling showed that mA enhances immune-associated translation by binding to the ECT2/3/4 readers. We propose that mA 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.