The cellular response to general and programmed DNA double strand breaks

被引:234
作者
Bassing, CH
Alt, FW [1 ]
机构
[1] Harvard Univ, Sch Med, Dept Genet, CBR Inst Biomed Res,Childrens Hosp, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Genet, Howard Hughes Med Inst,Childrens Hosp, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
cellular response; DNA double strand breaks; eukaryotic cells;
D O I
10.1016/j.dnarep.2004.06.001
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
DNA double strand breaks (DSBs) are among the most dangerous lesions that can occur in the genome of eukaryotic cells. Proper repair of chromosomal DSBs is critical for maintaining cellular viability and genomic integrity and, in multi-cellular organisms, for suppression of tumorigenesis. Thus, eukaryotic cells have evolved specialized and redundant molecular mechanisms to sense, respond to, and repair DSBs. in this chapter, we provide an overview of the progress that has been made over the last decade in elucidating the identity and function of components that participate in the cellular response to chromosomal DSBs. Then, we discuss, in more depth, the response to DSBs that occur in the context of the V(D)J recombination and IgH class switch recombination reactions that occur in cells of the lymphocyte lineage. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:781 / 796
页数:16
相关论文
共 104 条
[81]  
ROONEY S, 2004, IN PRESS IMMNOL REV
[82]   Restraining the V(D)J recombinase [J].
Roth, DB .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (08) :656-666
[83]   Staggered AID-dependent DNA double strand breaks are the predominant DNA lesions targeted to Sμ in Ig class switch recombination [J].
Rush, JS ;
Fugmann, SD ;
Schatz, DG .
INTERNATIONAL IMMUNOLOGY, 2004, 16 (04) :549-557
[84]   Joining-deficient RAG1 mutants block V(D)J recombination in vivo and hairpin opening in vitro [J].
Schultz, HY ;
Landree, MA ;
Qiu, JX ;
Kale, SB ;
Roth, DB .
MOLECULAR CELL, 2001, 7 (01) :65-75
[85]   Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions [J].
Sharpless, NE ;
Ferguson, DO ;
O'Hagan, RC ;
Castrillon, DH ;
Lee, C ;
Farazi, PA ;
Alson, S ;
Fleming, J ;
Morton, CC ;
Frank, K ;
Chin, L ;
Alt, FW ;
DePinho, RA .
MOLECULAR CELL, 2001, 8 (06) :1187-1196
[86]   RAG-2-DEFICIENT MICE LACK MATURE LYMPHOCYTES OWING TO INABILITY TO INITIATE V(D)J REARRANGEMENT [J].
SHINKAI, Y ;
RATHBUN, G ;
LAM, KP ;
OLTZ, EM ;
STEWART, V ;
MENDELSOHN, M ;
CHARRON, J ;
DATTA, M ;
YOUNG, F ;
STALL, AM ;
ALT, FW .
CELL, 1992, 68 (05) :855-867
[87]   MDC1 is a mediator of the mammalian DNA damage checkpoint [J].
Stewart, GS ;
Wang, B ;
Bignell, CR ;
Taylor, AMR ;
Elledge, SJ .
NATURE, 2003, 421 (6926) :961-966
[88]   ATM and DNA-PK function redundantly to phosphorylate H2AX after exposure to ionizing radiation [J].
Stiff, T ;
O'Driscoll, M ;
Rief, N ;
Iwabuchi, K ;
Löbrich, M ;
Jeggo, PA .
CANCER RESEARCH, 2004, 64 (07) :2390-2396
[89]   Targeted disruption of the catalytic subunit of the DNA-PK gene in mice confers severe combined immunodeficiency and radiosensitivity [J].
Taccioli, GE ;
Amatucci, AG ;
Beamish, HJ ;
Gell, D ;
Xiang, XH ;
Arzayus, MIT ;
Priestley, A ;
Jackson, SP ;
Rothstein, AM ;
Jeggo, PA ;
Herrera, VLM .
IMMUNITY, 1998, 9 (03) :355-366
[90]   Nijmegen breakage syndrome gene, NBS1, and molecular links to factors for genome stability [J].
Tauchi, H ;
Matsuura, S ;
Kobayashi, J ;
Sakamoto, S ;
Komatsu, K .
ONCOGENE, 2002, 21 (58) :8967-8980