ArticleThe Journal of experimental medicine2016
DNA polymerase ι functions in the generation of tandem mutations during somatic hypermutation of antibody genes.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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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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.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation.Science China. Life sciences · 2024Review
- Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health.Molecular and cellular biology · 2023Article
- Enabling Inference for Context-Dependent Models of Mutation by Bounding the Propagation of Dependency.Journal of computational biology : a journal of computational molecular cell biology · 2022Article
- Promoter Proximity Defines Mutation Window for VJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Characterisation of the spectrum and genetic dependence of collateral mutations induced by translesion DNA synthesis.PLoS genetics · 2022Article
- Deep learning model of somatic hypermutation reveals importance of sequence context beyond hotspot targeting.iScience · 2022Article
- Tandem Substitutions in Somatic Hypermutation.Frontiers in immunology · 2021Article
- Mysterious and fascinating: DNA polymerase ɩ remains enigmatic 20 years after its discovery.DNA repair · 2020Review
- What Targets Somatic Hypermutation to the Immunoglobulin Loci?Viral immunology · 2020Review
- Women in immunology: 2020 and beyond.Nature immunology · 2020Review
- Large deletions in immunoglobulin genes are associated with a sustained absence of DNA Polymerase η.Scientific reports · 2020Article
- Clustered Mutations at the Murine and Human IgH Locus Exhibit Significant Linkage Consistent with Templated Mutagenesis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- POLE proofreading defects: Contributions to mutagenesis and cancer.DNA repair · 2019Review
- DNA polymerase ι is acetylated in response to SScientific reports · 2019Article
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- DNA polymerase η mutational signatures are found in a variety of different types of cancer.Cell cycle (Georgetown, Tex.) · 2018Article
- Mouse DNA polymerase ι lacking the forty-two amino acids encoded by exon-2 is catalytically inactive in vitro.DNA repair · 2017Article
- Evaluation of the Antigen-Experienced B-Cell Receptor Repertoire in Healthy Children and Adults.Frontiers in immunology · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
DNA polymerase ι (Pol ι) is an attractive candidate for somatic hypermutation in antibody genes because of its low fidelity. To identify a role for Pol ι, we analyzed mutations in two strains of mice with deficiencies in the enzyme: 129 mice with negligible expression of truncated Pol ι, and knock-in mice that express full-length Pol ι that is catalytically inactive. Both strains had normal frequencies and spectra of mutations in the variable region, indicating that loss of Pol ι did not change overall mutagenesis. We next examined if Pol ι affected tandem mutations generated by another error-prone polymerase, Pol ζ. The frequency of contiguous mutations was analyzed using a novel computational model to determine if they occur during a single DNA transaction or during two independent events. Analyses of 2,000 mutations from both strains indicated that Pol ι-compromised mice lost the tandem signature, whereas C57BL/6 mice accumulated significant amounts of double mutations. The results support a model where Pol ι occasionally accesses the replication fork to generate a first mutation, and Pol ζ extends the mismatch with a second mutation.
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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.