ERCC1公司
生物
染色体易位
核酸内切酶
分子生物学
核苷酸切除修复
核酸酶
DNA修复
DNA
同源重组
细胞生物学
遗传学
基因
作者
Wanyu Bai,Guangchao Zhu,Jiejie Xu,Pingyue Chen,Fei-Long Meng,Xue Hou,Chun Chen,Jing Dong
出处
期刊:Cell Reports
[Elsevier]
日期:2021-09-01
卷期号:36 (13): 109756-109756
被引量:14
标识
DOI:10.1016/j.celrep.2021.109756
摘要
Robust alternative end joining (A-EJ) in classical non-homologous end joining (c-NHEJ)-deficient murine cells features double-strand break (DSB) end resection and microhomology (MH) usage and promotes chromosomal translocation. The activities responsible for removing 3' single-strand overhangs following resection and MH annealing in A-EJ remain unclear. We show that, during class switch recombination (CSR) in mature mouse B cells, the structure-specific endonuclease complex XPF-ERCC1SLX4, although not required for normal CSR, represents a nucleotide-excision-repair-independent 3' flap removal activity for A-EJ-mediated CSR. B cells deficient in DNA ligase 4 and XPF-ERCC1 exhibit further impaired class switching, reducing joining to the resected S region DSBs without altering the MH pattern in S-S junctions. In ERCC1-deficient A-EJ cells, 3' single-stranded DNA (ssDNA) flaps that are generated predominantly in S/G2 phase of the cell cycle are susceptible to nuclease resolution. Moreover, ERCC1 promotes c-myc-IgH translocation in Lig4-/- cells. Our study reveals an important role of the flap endonuclease XPF-ERCC1 in A-EJ and oncogenic translocation in mouse B cells.
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