ArticleProceedings of the National Academy of Sciences of the United States of America2014
Differential regulation of S-region hypermutation and class-switch recombination by noncanonical functions of uracil DNA glycosylase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- TTC33 forms a complex with WDR61 and PHF5A to recruit factors relevant to genomic integrity.Nature communications · 2026Article
- UNG-RPA interaction governs the choice between high-fidelity and mutagenic uracil repair.Nucleic acids research · 2026Article
- R-loop disruption triggers irreversible topoisomerase 1-DNA cleavage complex formation during AID-dependent IgH gene diversification.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Trade-offs between receptor modification and fitness drive host-bacteriophage co-evolution leading to phage extinction or co-existence.The ISME journal · 2024Article
- Alternative end-joining in BCR gene rearrangements and translocations.Acta biochimica et biophysica Sinica · 2022Review
- Article
- SAMHD1-mediated dNTP degradation is required for efficient DNA repair during antibody class switch recombination.The EMBO journal · 2020Article
- The Essential Co-Option of Uracil-DNA Glycosylases by Herpesviruses Invites Novel Antiviral Design.Microorganisms · 2020Review
- Uracil-DNA glycosylase is not implicated in the choice of the DNA repair pathway during B-cell class switch recombination.Cellular & molecular immunology · 2019Article
- DNA double-strand break response factors influence end-joining features of IgH class switch and general translocation junctions.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Kin17 facilitates multiple double-strand break repair pathways that govern B cell class switching.Scientific reports · 2016Article
- Uracil DNA glycosylase interacts with the p32 subunit of the replication protein A complex to modulate HIV-1 reverse transcription for optimal virus dissemination.Retrovirology · 2016Article
- Identification of DNA cleavage- and recombination-specific hnRNP cofactors for activation-induced cytidine deaminase.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- B cell Rab7 mediates induction of activation-induced cytidine deaminase expression and class-switching in T-dependent and T-independent antibody responses.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- APE1 is dispensable for S-region cleavage but required for its repair in class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Opinion: uracil DNA glycosylase (UNG) plays distinct and non-canonical roles in somatic hypermutation and class switch recombination.International immunology · 2014Review
Corrections and comments
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5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation-induced cytidine deaminase (AID) is essential to class-switch recombination (CSR) and somatic hypermutation (SHM) in both V region SHM and S region SHM (s-SHM). Uracil DNA glycosylase (UNG), a member of the base excision repair (BER) complex, is required for CSR. Strikingly, however, UNG deficiency causes augmentation of SHM, suggesting involvement of distinct functions of UNG in SHM and CSR. Here, we show that noncanonical scaffold functions of UNG regulate s-SHM negatively and CSR positively. The s-SHM suppressive function of UNG is attributed to the recruitment of faithful BER components at the cleaved DNA locus, with competition against error-prone polymerases. By contrast, the CSR-promoting function of UNG enhances AID-dependent S-S synapse formation by recruiting p53-binding protein 1 and DNA-dependent protein kinase, catalytic subunit. Several loss-of-catalysis mutants of UNG discriminated CSR-promoting activity from s-SHM suppressive activity. Taken together, the noncanonical function of UNG regulates the steps after AID-induced DNA cleavage: error-prone repair suppression in s-SHM and end-joining promotion in CSR.
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