ArticleNucleic acids research2016
Non-canonical uracil processing in DNA gives rise to double-strand breaks and deletions: relevance to class switch recombination.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Zebrafish Unga Is Required for Genomic Maintenance upon Genotoxic Stress and Male Fertility.Journal of developmental biology · 2025Article
- Nucleotide level mapping of uracils in murine heavy chain switch regions shows correlation between uracilation and positions of switch junctions created during class-switch recombination.NAR molecular medicine · 2025Article
- APE2 Promotes AID-Dependent Somatic Hypermutation in Primary B Cell Cultures That Is Suppressed by APE1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- NONO phase separation enhances DNA damage repair by accelerating nuclear EGFR-induced DNA-PK activation.American journal of cancer research · 2021Article
- 53BP1: a DSB escort.Genes & development · 2020Review
- R-loops: targets for nuclease cleavage and repeat instability.Current genetics · 2018Review
- Main steps in DNA double-strand break repair: an introduction to homologous recombination and related processes.Chromosoma · 2018Review
- Cytosine deamination and base excision repair cause R-loop-induced CAG repeat fragility and instability inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- MBD4 Facilitates Immunoglobulin Class Switch Recombination.Molecular and cellular biology · 2017Article
- Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases.Chemical reviews · 2016Review
- UNG protects B cells from AID-induced telomere loss.The Journal of experimental medicine · 2016Article
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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
During class switch recombination (CSR), antigen-stimulated B-cells rearrange their immunoglobulin constant heavy chain (CH) loci to generate antibodies with different effector functions. CSR is initiated by activation-induced deaminase (AID), which converts cytosines in switch (S) regions, repetitive sequences flanking the CH loci, to uracils. Although U/G mispairs arising in this way are generally efficiently repaired to C/Gs by uracil DNA glycosylase (UNG)-initiated base excision repair (BER), uracil processing in S-regions of activated B-cells occasionally gives rise to double strand breaks (DSBs), which trigger CSR. Surprisingly, genetic experiments revealed that CSR is dependent not only on AID and UNG, but also on mismatch repair (MMR). To elucidate the role of MMR in CSR, we studied the processing of uracil-containing DNA substrates in extracts of MMR-proficient and -deficient human cells, as well as in a system reconstituted from recombinant BER and MMR proteins. Here, we show that the interplay of these repair systems gives rise to DSBs in vitro and to genomic deletions and mutations in vivo, particularly in an S-region sequence. Our findings further suggest that MMR affects pathway choice in DSB repair. Given its amenability to manipulation, our system represents a powerful tool for the molecular dissection of CSR.
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