X-ray repair cross-complementing protein 1 (XRCC1) deficiency enhances class switch recombination and is permissive for alternative end joining

被引:24
|
作者
Han, Li [1 ]
Mao, Weifeng [1 ]
Yu, Kefei [1 ]
机构
[1] Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA
基金
美国国家卫生研究院;
关键词
DNA-LIGASE III; V(D)J RECOMBINATION; BREAK REPAIR; PATHWAY; ABSENCE; TRANSLOCATIONS; MECHANISM; CELLS; KU70; IV;
D O I
10.1073/pnas.1120743109
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
DNA double-strand breaks (DSBs) are essential intermediates in Ig gene rearrangements: V(D)J and class switch recombination (CSR). In contrast to V(D) J recombination, which is almost exclusively dependent on nonhomologous end joining (NHEJ), CSR can occur in NHEJ-deficient cells via a poorly understand backup pathway (or pathways) often termed alternative end joining (A-EJ). Recently, several components of the single-strand DNA break (SSB) repair machinery, including XRCC1, have been implicated in A-EJ. To determine its role in A-EJ and CSR, Xrcc1 was deleted by targeted mutation in the CSR proficient mouse B-cell line, CH12F3. Here we demonstrate that XRCC1 deficiency slightly increases the efficiency of CSR. More importantly, Lig4 and XRCC1 double-deficient cells switch as efficiently as Lig4-deficient cells, clearly indicating that XRCC1 is dispensable for A-EJ in CH12F3 cells during CSR.
引用
收藏
页码:4604 / 4608
页数:5
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