ArticleMolecular and cellular biology2009
The concerted action of Msh2 and UNG stimulates somatic hypermutation at A . T base pairs.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Repertoire Sequencing of B Cells Elucidates the Role of UNG and Mismatch Repair Proteins in Somatic Hypermutation in Humans.Frontiers in immunology · 2019Pooled it
- MKLN1-dependent GID4/CTLH E3 ubiquitin ligase complex assemblies are required to support B-cell antibody diversification.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Modular cytosine base editing promotes epigenomic and genomic modifications.Nucleic acids research · 2024Article
- HMCES protects immunoglobulin genes specifically from deletions during somatic hypermutation.Genes & development · 2022Article
- AID in Antibody Diversification: There and Back Again.Trends in immunology · 2020Review
- Correlations in Somatic Hypermutation Between Sites in IGHV Genes Can Be Explained by Interactions Between AID and/or Polη Hotspots.Frontiers in immunology · 2020Article
- AID Overlapping and Polη Hotspots Are Key Features of Evolutionary Variation Within the Human Antibody Heavy Chain (IGHV) Genes.Frontiers in immunology · 2020Article
- SAMHD1 enhances immunoglobulin hypermutation by promoting transversion mutation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- JMolecular immunology · 2018Article
- Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2.Nucleic acids research · 2017Article
- Pms2 and uracil-DNA glycosylases act jointly in the mismatch repair pathway to generate Ig gene mutations at A-T base pairs.The Journal of experimental medicine · 2017Article
- Overlapping hotspots in CDRs are critical sites for V region diversification.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Differential expression of APE1 and APE2 in germinal centers promotes error-prone repair and A:T mutations during somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The dual nature of mismatch repair as antimutator and mutator: for better or for worse.Frontiers in genetics · 2014Review
- DNA polymerases β and λ do not directly affect Ig variable region somatic hypermutation although their absence reduces the frequency of mutations.DNA repair · 2013Article
- Elevated incidence of polyp formation in APC(Min/⁺)Msh2⁻/⁻ mice is independent of nitric oxide-induced DNA mutations.PloS one · 2013Article
- Does DNA repair occur during somatic hypermutation?Seminars in immunology · 2012Review
- AIDing antibody diversity by error-prone mismatch repair.Seminars in immunology · 2012Review
- Negative supercoiling creates single-stranded patches of DNA that are substrates for AID-mediated mutagenesis.PLoS genetics · 2012Article
- DNA glycosylases: in DNA repair and beyond.Chromosoma · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mismatch repair plays an essential role in reducing the cellular mutation load. Paradoxically, proteins in this pathway produce A . T mutations during the somatic hypermutation of immunoglobulin genes. Although recent evidence implicates the translesional DNA polymerase eta in producing these mutations, it is unknown how this or other translesional polymerases are recruited to immunoglobulin genes, since these enzymes are not normally utilized in conventional mismatch repair. In this report, we demonstrate that A . T mutations were closely associated with transversion mutations at a deoxycytidine. Furthermore, deficiency in uracil-N-glycolase (UNG) or mismatch repair reduced this association. These data reveal a previously unknown interaction between the base excision and mismatch repair pathways and indicate that an abasic site generated by UNG within the mismatch repair tract recruits an error-prone polymerase, which then introduces A . T mutations. Our analysis further indicates that repair tracts typically are approximately 200 nucleotides long and that polymerase eta makes approximately 1 error per 300 T nucleotides. The concerted action of Msh2 and UNG in stimulating A . T mutations also may have implications for mutagenesis at sites of spontaneous cytidine deamination.
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