ArticleProceedings of the National Academy of Sciences of the United States of America2004
Naturally occurring H-DNA-forming sequences are mutagenic in mammalian cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 193 citations in OpenAlex.
- HSeeker: an algorithm for systematic H-DNA sequence identification.bioRxiv : the preprint server for biology · 2026Article
- Oxidative DNA Damage Exacerbates the Mutagenic Potential of Alternative DNA Structures via Altered DNA Repair Processing.Environmental and molecular mutagenesis · 2026Article
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Base excision repair within structure-forming repeat sequences and its impact on cancer and other diseases.NAR cancer · 2025Review
- Aging alters genomic instability at endogenous mutation hotspots in mice.Scientific reports · 2025Article
- Triplexes Color the Chromaverse by Modulating Nucleosome Phasing and Anchoring Chromatin Condensates.International journal of molecular sciences · 2025Review
- Ribosomal DNA arrays are the most H-DNA rich element in the human genome.NAR genomics and bioinformatics · 2025Article
- Oxidative damage within alternative DNA structures results in aberrant mutagenic processing.Nucleic acids research · 2025Article
- Article
- Chemoproteomic profiling unveils binding and functional diversity of endogenous proteins that interact with endogenous triplex DNA.Nature chemistry · 2024Article
- Triplex H-DNA structure: the long and winding road from the discovery to its role in human disease.NAR molecular medicine · 2024Article
- Obesity increases genomic instability at DNA repeat-mediated endogenous mutation hotspots.Nature communications · 2024Article
- Article
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- Understanding intercalative modulation of G-rich sequence folding: solution structure of a TINA-conjugated antiparallel DNA triplex.Nucleic acids research · 2024Article
- MoCoLo: a testing framework for motif co-localization.Briefings in bioinformatics · 2024Article
- Detection of alternative DNA structures and its implications for human disease.Molecular cell · 2023Review
- Dynamic alternative DNA structures in biology and disease.Nature reviews. Genetics · 2023Review
- Methods to Study Z-DNA-Induced Genetic Instability.Methods in molecular biology (Clifton, N.J.) · 2023Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Naturally occurring DNA sequences can form noncanonical structures such as H-DNA, which are abundant and regulate the expression of several disease-linked genes. Here, we show that H-DNA-forming sequences are intrinsically mutagenic in mammalian cells. This finding suggests that DNA is a causative factor in mutagenesis and not just the end product. By using the endogenous H-DNA-forming sequence found in the human c-myc promoter, mutation frequencies in a reporter gene were increased approximately 20-fold over background in COS-7 cells. H-DNA-induced double-strand breaks (DSBs) were detected near the H-DNA locus. The structures of the mutants revealed microhomologies at the breakpoints, consistent with a nonhomologous end-joining repair of the DSBs. These results implicate H-DNA-induced DSBs in c-myc gene translocations in diseases such as Burkitt's lymphoma and t(12;15) BALB/c plasmacytomas, where most breakpoints are found near the H-DNA-forming site. Thus, our findings suggest that H-DNA is a source of genetic instability resulting from DSBs and demonstrate that naturally occurring DNA sequences are mutagenic in mammals, perhaps contributing to genetic evolution and disease.
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