ArticleMolecular cell2023
Exclusion of m6A from splice-site proximal regions by the exon junction complex dictates m6A topologies and mRNA stability.
Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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Who cites it
119 citing papers in PubMed, 194 citations in OpenAlex.
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- The stability of m6A-marked transcripts is linked to cell identity in planarians.Nucleic acids research · 2026Article
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- VeloRM: disentangling pre- and post-splicing RNA modification dynamics at single-cell resolution.Nucleic acids research · 2026Article
- Regulatory elements on chromatin-associated RNA 15 years beyond RNA epigenetics.Nature chemical biology · 2026Review
- Transcription Start Site Choice Regulates mGenes · 2026Article
- CDS-localized mNature plants · 2026Article
- Non-coding RNAs in lipid metabolism and their roles in atherosclerosis.Nature reviews. Cardiology · 2026Review
- Isoform-specific m6A deposition and coordinated splicing shape mammalian transcriptome evolution.Nature communications · 2026Article
- Systematic identification of tissue-conserved mbioRxiv : the preprint server for biology · 2026Article
- Seven wonders of RNA modification biology.RNA (New York, N.Y.) · 2026Review
- High-stoichiometry mRNA (New York, N.Y.) · 2026Article
- NNature reviews. Cancer · 2026Review
- Single-nucleotide m⁶A mapping uncovers redundant YTHDF function in planarian progenitor fate selection.The EMBO journal · 2026Article
- Mechanisms at the Intersection of lncRNA and m6A Biology.Non-coding RNA · 2026Review
59 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.