As the most abundant internal modification of mRNA, N -methyladenosine (m A) methylation of RNA is emerging as a new layer of epitranscriptomic gene regulation in cellular processes, including embryo development, flowering-time control, microspore generation and fruit ripening, in plants. However, the cellular role of m A in plant responses to environmental stimuli remains largely unexplored. In this study, we show that m A methylation plays an important role in salt stress tolerance in Arabidopsis. All mutants of m A writer components, including MTA, MTB, VIRILIZER (VIR) and HAKAI, displayed salt-sensitive phenotypes in an m A-dependent manner. The vir mutant, in which the level of m A was most highly reduced, exhibited salt-hypersensitive phenotypes. Analysis of the m A methylome in the vir mutant revealed a transcriptome-wide loss of m A modification in the 3' untranslated region (3'-UTR). We demonstrated further that VIR-mediated m A methylation modulates reactive oxygen species homeostasis by negatively regulating the mRNA stability of several salt stress negative regulators, including ATAF1, GI and GSTU17, through affecting 3'-UTR lengthening linked to alternative polyadenylation. Our results highlight the important role played by epitranscriptomic mRNA methylation in the salt stress response of Arabidopsis and indicate a strong link between m A methylation and 3'-UTR length and mRNA stability during stress adaptation.