ArticleProceedings of the National Academy of Sciences of the United States of America2009
Interference of mismatch and base excision repair during the processing of adjacent U/G mispairs may play a key role in somatic hypermutation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 81 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 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
- MKLN1-dependent GID4/CTLH E3 ubiquitin ligase complex assemblies are required to support B-cell antibody diversification.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Genotoxic effects of base and prime editing in human hematopoietic stem cells.Nature biotechnology · 2024Article
- DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023Review
- CNOT6: A Novel Regulator of DNA Mismatch Repair.Cells · 2022Article
- The threat of programmed DNA damage to neuronal genome integrity and plasticity.Nature genetics · 2022Review
- CRISPR-based genome editing through the lens of DNA repair.Molecular cell · 2022Review
- Dynamics of Mismatch and Alternative Excision-Dependent Repair in ReplicatingFrontiers in microbiology · 2022Article
- Article
- Detection of Genomic Uracil Patterns.International journal of molecular sciences · 2021Review
- Intrinsic Strand-Incision Activity of Human UNG: Implications for Nick Generation in Immunoglobulin Gene Diversification.Frontiers in immunology · 2021Article
- 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
- AID Overlapping and Polη Hotspots Are Key Features of Evolutionary Variation Within the Human Antibody Heavy Chain (IGHV) Genes.Frontiers in immunology · 2020Article
- Synthetic lethality between BRCA1 deficiency and poly(ADP-ribose) polymerase inhibition is modulated by processing of endogenous oxidative DNA damage.Nucleic acids research · 2019Article
- The Camel Adaptive Immune Receptors Repertoire as a Singular Example of Structural and Functional Genomics.Frontiers in genetics · 2019Review
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- SAMHD1 enhances immunoglobulin hypermutation by promoting transversion mutation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- No Overt Clinical Immunodeficiency Despite Immune Biological Abnormalities in Patients With Constitutional Mismatch Repair Deficiency.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In eukaryotic mismatch repair (MMR), degradation of the error-containing strand initiates at nicks or gaps that can be up to a kilobase away from the mispair. These discontinuities may be the ends of Okazaki fragments or the 3'-termini of the leading strands during replication, whereas the termini of invading strands may fulfill this role during recombination. Here we show that, in extracts of human cells, MMR can initiate also at sites of ongoing base excision repair. Although unlikely under normal circumstances, this situation may arise in vivo during somatic hypermutation (SHM) and class switch recombination of Ig genes, where activation-induced cytidine deaminase (AID) generates multiple U/G mismatches in the variable or switch regions. Uracil should normally be excised by base excision repair (BER), but we show here that MMR proteins activated by a nearby mismatch interfere with uracil processing to generate long single-stranded gaps. We postulate that, in a subset of the repair events, filling-in of the MMR-generated gaps might be catalyzed by the error-prone polymerase-eta, rather than by the high-fidelity polymerase-delta. Because polymerase-eta has a propensity to misinsertions opposite adenine residues, the above mechanism would help explain why SHM affects not only C/G, but also A/T base pairs.
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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.