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

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, Xiaoming Wang, Wei Xiao and Fei-Long Meng ()
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Dingpeng Yang: Shanghai Institute of Biochemistry and Cell Biology, 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
Xia Xie: Shanghai Institute of Biochemistry and Cell Biology, 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
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
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

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-16632-8

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