N6-methyladenosine (m6A), a widespread destabilizing mark on mRNA, is non-uniformly distributed across the transcriptome, yet the basis for its selective deposition is unknown. Here, we propose that m6A deposition is not selective. Instead, it is exclusion based: m6A consensus motifs are methylated by default, unless they are within a window of ∼100 nt from a splice junction. A simple model which we extensively validate, relying exclusively on presence of m6A motifs and exon-intron architecture, allows in silico recapitulation of experimentally measured m6A profiles. We provide evidence that exclusion from splice junctions is mediated by the exon junction complex (EJC), potentially via physical occlusion, and that previously observed associations between exon-intron architecture and mRNA decay are mechanistically mediated via m6A. Our findings establish a mechanism coupling nuclear mRNA splicing and packaging with the covalent installation of m6A, in turn controlling cytoplasmic decay. [Display omitted] • m6A is deposited by default at DRACH motifs but excluded from splice-site proximity • Simple model based on above principles in silico reconstructs m6A landscapes • Exclusion from splice-junction proximity is mediated via exon junction complex • m6A is memory of nuclear splicing dictating cytoplasmic stability Uzonyi et al. find that m6A is introduced by default at all eligible consensus motifs, except near splice sites, where it is occluded via the exon junction complex. A simple model, relying on motif availability and splice-site distance in silico reconstructs m6A topologies. m6A links exon-intron architecture with cytoplasmic fate. [ABSTRACT FROM AUTHOR]