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REV7 is required for processing AID initiated DNA lesions in activated B cells

Author

Listed:
  • Dingpeng Yang

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Ying Sun

    (Capital Normal University)

  • Jingjing Chen

    (Nanjing Medical University)

  • Ying Zhang

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences)

  • Shuangshuang Fan

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences)

  • Min Huang

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Xia Xie

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Yanni Cai

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences)

  • Yafang Shang

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Tuantuan Gui

    (Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine)

  • Liming Sun

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Jiazhi Hu

    (School of Life Sciences, Peking-Tsinghua Center for Life Sciences, Peking University)

  • Junchao Dong

    (Zhongshan School of Medicine, Sun Yat-sen University)

  • Leng-Siew Yeap

    (Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine)

  • Xiaoming Wang

    (Nanjing Medical University)

  • Wei Xiao

    (Capital Normal University)

  • Fei-Long Meng

    (Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

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.

Suggested Citation

  • Dingpeng Yang & Ying Sun & Jingjing Chen & Ying Zhang & Shuangshuang Fan & Min Huang & Xia Xie & Yanni Cai & Yafang Shang & Tuantuan Gui & Liming Sun & Jiazhi Hu & Junchao Dong & Leng-Siew Yeap & Xiao, 2020. "REV7 is required for processing AID initiated DNA lesions in activated B cells," Nature Communications, Nature, vol. 11(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-16632-8
    DOI: 10.1038/s41467-020-16632-8
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