ArticleNucleic acids research2021
Human MettL3-MettL14 RNA adenine methyltransferase complex is active on double-stranded DNA containing lesions.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 73 citations in OpenAlex.
- METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review).International journal of oncology · 2026Review
- Role of the DNA methyltransferases in diabetes mellitus and Its complications.Molecular biology reports · 2026Review
- Rewriting the RNA code: an mFrontiers in immunology · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Inhibition ofACS omega · 2025Article
- Mechanism for the substrate recognition by a eukaryotic DNA NNature communications · 2025Article
- YTHDF3 recognizes DNA N6-methyladenine and recruits ALKBH1 for 6mA removal from genomic DNA.The EMBO journal · 2025Article
- Inhibition ofbioRxiv : the preprint server for biology · 2025Article
- The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025Review
- Poly-(ADP-ribose) serves as a scaffold for the methyltransferase METTL3/14 complex in the DNA damage response.Nucleic acids research · 2025Article
- Article
- YTHDC1 negatively regulates UBE3A to influence RAD51 ubiquitination and inhibit apoptosis in colorectal cancer cells.Scientific reports · 2025Article
- DNA damage-induced YTHDC1 O-GlcNAcylation promotes homologous recombination by enhancing mFundamental research · 2025Article
- Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.European journal of medical research · 2025Review
- Cap-specific terminal N6-methyladeonsine methylation of RNA mediated by PCIF1 and possible therapeutic implications.Genes & diseases · 2025Review
- Structures and mechanisms of the RNA mActa biochimica et biophysica Sinica · 2024Review
- Liver-specific Mettl14 deletion induces nuclear heterotypia and dysregulates RNA export machinery.bioRxiv : the preprint server for biology · 2024Article
- RNA methylation patterns, immune characteristics, and autophagy-related mechanisms mediated by N6-methyladenosine (m6A) regulatory factors in venous thromboembolism.BMC genomics · 2024Article
- Article
- Epigenetic marks or not? The discovery of novel DNA modifications in eukaryotes.The Journal of biological chemistry · 2024Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
MettL3-MettL14 methyltransferase complex has been studied widely for its role in RNA adenine methylation. This complex is also recruited to UV- and X-ray exposed DNA damaged sites, and its methyltransfer activity is required for subsequent DNA repair, though in theory this could result from RNA methylation of short transcripts made at the site of damage. We report here that MettL3-MettL14 is active in vitro on double-stranded DNA containing a cyclopyrimidine dimer - a major lesion of UV radiation-induced products - or an abasic site or mismatches. Furthermore, N6-methyladenine (N6mA) decreases misincorporation of 8-oxo-guanine (8-oxoG) opposite to N6mA by repair DNA polymerases. When 8-oxoG is nevertheless incorporated opposite N6mA, the methylation inhibits N6mA excision from the template (correct) strand by the adenine DNA glycosylase (MYH), implying that the methylation decreases inappropriate misrepair. Finally, we observed that the N6mA reader domain of YTHDC1, which is also recruited to sites of DNA damage, binds N6mA that is located across from a single-base gap between two canonical DNA helices. This YTHDC1 complex with a gapped duplex is structurally similar to DNA complexes with FEN1 and GEN1 - two members of the nuclease family that act in nucleotide excision repair, mismatch repair and homologous recombination, and which incise distinct non-B DNA structures. Together, the parts of our study provide a plausible mechanism for N6mA writer and reader proteins acting directly on lesion-containing DNA, and suggest in vivo experiments to test the mechanisms involving methylation of adenine.
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Registered trials
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.