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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.


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, Fei-Long Meng. REV7 is required for processing AID initiated DNA lesions in activated B cells. Nature communications. 2020 Jun 04;11(1):2812

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PMID: 32499490

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