ArticleeLife2014
Repair of naturally occurring mismatches can induce mutations in flanking DNA.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 101 citations in OpenAlex.
- Leveraging base excision repair for efficient adenine base editing of mitochondrial DNA.Nature biotechnology · 2026Article
- Genotype-dependent DNA methylation patterns are negatively associated with allelic variation rather than heat-induced gene expression in two contrasting potato genotypes.The Plant journal : for cell and molecular biology · 2026Article
- Reprogramming tumor immunity through APOBEC3s-mediated mutagenesis: from genome instability to immune checkpoint interactions.Frontiers in immunology · 2026Review
- Action-at-a-distance mutations by 8-oxo-7,8-dihydroguanine: adenine pair triggered by MUTYH.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Article
- APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice.Cancer reports (Hoboken, N.J.) · 2025Article
- Untargeted Mutation Triggered by Ribonucleoside Embedded in DNA.International journal of molecular sciences · 2024Article
- Mutations atMolecular and cellular biology · 2024Article
- Spectrum of DNA mismatch repair failures viewed through the lens of cancer genomics and implications for therapy.Clinical science (London, England : 1979) · 2022Article
- RepairSig: Deconvolution of DNA damage and repair contributions to the mutational landscape of cancer.Cell systems · 2021Article
- The origin of human mutation in light of genomic data.Nature reviews. Genetics · 2021Review
- Eliminating base-editor-induced genome-wide and transcriptome-wide off-target mutations.Nature cell biology · 2021Article
- Loss of the abasic site sensor HMCES is synthetic lethal with the activity of the APOBEC3A cytosine deaminase in cancer cells.PLoS biology · 2021Article
- Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability.Expert opinion on therapeutic targets · 2021Review
- Updated Understanding of Cancer as a Metabolic and Telomere-Driven Disease, and Proposal for Complex Personalized Treatment, a Hypothesis.International journal of molecular sciences · 2020Review
- DNA mismatch repair promotes APOBEC3-mediated diffuse hypermutation in human cancers.Nature genetics · 2020Article
- Cytosine Methylation Affects the Mutability of Neighboring Nucleotides in Germline and Soma.Genetics · 2020Article
- Perturbation of base excision repair sensitizes breast cancer cells to APOBEC3 deaminase-mediated mutations.eLife · 2020Article
- Variation in base composition underlies functional and evolutionary divergence in non-LTR retrotransposons.Mobile DNA · 2020Article
- Epimutations in Developmental Genes Underlie the Onset of Domestication in Farmed European Sea Bass.Molecular biology and evolution · 2019Article
- A Quantitative Model Explains Single-Cell Dynamics of the Adaptive Response in Escherichia coli.Biophysical journal · 2019Article
Corrections and comments
- Commented on by
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
'Normal' genomic DNA contains hundreds of mismatches that are generated daily by the spontaneous deamination of C (U/G) and methyl-C (T/G). Thus, a mutagenic effect of their repair could constitute a serious genetic burden. We show here that while mismatches introduced into human cells on an SV40-based episome were invariably repaired, this process induced mutations in flanking DNA at a significantly higher rate than no mismatch controls. Most mutations involved the C of TpC, the substrate of some single strand-specific APOBEC cytidine deaminases, similar to the mutations that can typify the 'mutator phenotype' of numerous tumors. siRNA knockdowns and chromatin immunoprecipitation showed that TpC preferring APOBECs mediate the mutagenesis, and siRNA knockdowns showed that both the base excision and mismatch repair pathways are involved. That naturally occurring mispairs can be converted to mutators, represents an heretofore unsuspected source of genetic changes that could underlie disease, aging, and evolutionary change.DOI: http://dx.doi.org/10.7554/eLife.02001.001.
Indexed as
Identifiers
What OpenQuestion holds
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.