ArticleNature communications2020
REV7 is required for processing AID initiated DNA lesions in activated B cells.
Article in Nature communications, 2020. 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, 15 citations in OpenAlex.
- CFP1 promotes B cell class switch recombination through the regulation of S region germline transcription and proliferation.iScience · 2026Article
- CFP1 promotes germinal center affinity maturation and restrains memory B cell differentiation through H3K4me3 modulation.Nature communications · 2025Article
- USP25 Elevates SHLD2-Mediated DNA Double-Strand Break Repair and Regulates Chemoresponse in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- C-to-G editing generates double-strand breaks causing deletion, transversion and translocation.Nature cell biology · 2024Article
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- Attempts to evaluate locus suicide recombination and its potential role in B cell negative selection in the mouse.Frontiers in immunology · 2023Article
- Altered Phenotype and Enhanced Antibody-Producing Ability of Peripheral B Cells in Mice withCells · 2022Article
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- Molecular mechanisms of assembly and TRIP13-mediated remodeling of the human Shieldin complex.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- Single-Cell RNA Analysis Reveals Reduced Frequency and Activity of CXCR5XenotransplantationArticle
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation-induced cytidine deaminase (AID) initiates both antibody class switch recombination (CSR) and somatic hypermutation (SHM) in antibody diversification. DNA double-strand break response (DSBR) factors promote rearrangement in CSR, while translesion synthesis (TLS) polymerases generate mutations in SHM. REV7, a component of TLS polymerase zeta, is also a downstream effector of 53BP1-RIF1 DSBR pathway. Here, we study the multi-functions of REV7 and find that REV7 is required for the B cell survival upon AID-deamination, which is independent of its roles in DSBR, G2/M transition or REV1-mediated TLS. The cell death in REV7-deficient activated B cells can be fully rescued by AID-deficiency in vivo. We further identify that REV7-depedent TLS across UNG-processed apurinic/apyrimidinic sites is required for cell survival upon AID/APOBEC deamination. This study dissects the multiple roles of Rev7 in antibody diversification, and discovers that TLS is not only required for sequence diversification but also B cell survival upon AID-initiated lesions.
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