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

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Yang D,Sun Y,Chen J,Zhang Y,Fan S,Huang M,Xie X,Cai Y,Shang Y,Gui T,Sun L,Hu J,Dong J,Yeap LS,Wang X,Xiao W,Meng FL

doi

10.1038/s41467-020-16632-8

subject

Has Abstract

pub_date

2020-06-04 00:00:00

pages

2812

issue

1

issn

2041-1723

pii

10.1038/s41467-020-16632-8

journal_volume

11

pub_type

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