Regulation of homologous recombinational repair by lamin B1 in radiation-induced DNA damage

被引:25
作者
Liu, Ning-Ang [1 ]
Sun, Jiying [1 ]
Kono, Kazuteru [1 ]
Horikoshi, Yasunori [1 ,2 ]
Ikura, Tsuyoshi [3 ]
Tong, Xing [4 ]
Haraguchi, Tokuko [5 ]
Tashiro, Satoshi [1 ,2 ]
机构
[1] Hiroshima Univ, Res Inst Radiat Biol & Med, Dept Cellular Biol, Hiroshima, Hiroshima 7348553, Japan
[2] Hiroshima Univ, Res Ctr Math Chromatin Live Dynam RcMcD, Hiroshima, Hiroshima 7348553, Japan
[3] Kyoto Univ, Ctr Radiat Biol, Dept Mutagenesis, Lab Chromatin Dynam, Kyoto, Japan
[4] Soochow Univ, Coll Med, Lab Ctr, Suzhou, Peoples R China
[5] Natl Inst Informat & Commun Technol, Adv ICT Res Inst Kobe, Kobe, Hyogo, Japan
关键词
B-type lamins; nuclear envelope; progeria syndrome; RAD51; recombinational DNA repair; STRAND BREAK REPAIR; A-TYPE LAMINS; RAD51; GENE; CELL-CYCLE; DEFECTIVE MATURATION; NUCLEAR LAMINS; EXPRESSION; PROGERIA; PROTEIN; ORGANIZATION;
D O I
10.1096/fj.14-265546
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
DNA double-strand breaks (DSBs) are the major lethal lesion induced by ionizing radiation (IR). RAD51-dependent homologous recombination (HR) is one of the most important pathways in DSB repair and genome integrity maintenance. However, the mechanism of HR regulation by RAD51 remains unclear. To understand the mechanism of RAD51-dependent HR, we searched for interacting partners of RAD51 by a proteomics analysis and identified lamin B1 in human cells. Lamins are nuclear lamina proteins that play important roles in the structural organization of the nucleus and the regulation of chromosome functions. Immunoblotting analyses revealed that siRNA-mediated lamin B1 depletion repressed the DNA damage-dependent increase of RAD51 after IR. The repression was abolished by the proteasome inhibitor MG132, suggesting that lamin B1 stabilizes RAD51 by preventing proteasome-mediated degradation in cells with IR-induced DNA damage. We also showed that lamin B1 depletion repressed RAD51 focus formation and decreased the survival rates after IR. On the basis of these results, we propose that lamin B1 promotes DSB repair and cell survival by maintaining the RAD51 protein levels for HR upon DSB induction after IR.
引用
收藏
页码:2514 / 2525
页数:12
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