Differential usage of non-homologous end-joining and homologous recombination in double strand break repair

被引：370

作者：

Sonoda, Eiichiro ^{[1
]}

Hochegger, Helfrid ^{[1
]}

Saberi, Alihossein ^{[1
]}

Taniguchi, Yoshihito ^{[1
]}

Takeda, Shunichi ^{[1
]}

机构：

[1] Kyoto Univ, Grad Sch Med, Sakyo Ku, Kyoto 6068501, Japan

来源：

DNA REPAIR | 2006年 / 5卷 / 9-10期

关键词：

DSB; HR; NHEJ; Ku70; DT40;

D O I：

10.1016/j.dnarep.2006.05.022

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Repair of DNA double strand breaks (DSBs) plays a critical role in the maintenance of the genome. DSB arise frequently as a consequence of replication fork stalling and also due to the attack of exogenous agents. Repair of broken DNA is essential for survival. Two major pathways, homologous recombination (HR) and non-homologous end-joining (NHEJ) have evolved to deal with these lesions, and are conserved from yeast to vertebrates. Despite the conservation of these pathways, their relative contribution to DSB repair varies greatly between these two species. HR plays a dominant role in any DSB repair in yeast, whereas NHEJ significantly contributes to DSB repair in vertebrates. This active NHEJ requires a regulatory mechanism to choose HR or NHEJ in vertebrate cells. In this review, we illustrate how HR and NHEJ are differentially regulated depending on the phase of cell cycle and on the nature of the DSB. (c) 2006 Elsevier B.V. All rights reserved.

引用

页码：1021 / 1029

页数：9

共 62 条

[1] Loss of nonhomologous end joining confers camptothecin resistance in DT40 cells - Implications for the repair of topoisomerase I-mediated DNA damage [J].

Adachi, N ;

So, SR ;

Koyama, H .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (36) :37343-37348

[2] DNA ligase IV-deficient cells are more resistant to ionizing radiation in the absence of Ku70: Implications for DNA double-strand break repair [J].

Adachi, N ;

Ishino, T ;

Ishii, Y ;

Takeda, S ;

Koyama, H .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (21) :12109-12113

[3] The PARP superfamily [J].

Amé, JC ;

Spenlehauer, C ;

de Murcia, G .

BIOESSAYS, 2004, 26 (08) :882-893

[4]

AME JC, PARP 2 NOVEL MAMMALI

[5] Suppression of the poly(ADP-ribose) polymerase activity by DNA-dependent protein kinase in vitro [J].

Ariumi, Y ;

Masutani, M ;

Copeland, TD ;

Mimori, T ;

Sugimura, T ;

Shimotohno, K ;

Ueda, K ;

Hatanaka, M ;

Noda, M .

ONCOGENE, 1999, 18 (32) :4616-4625

[6] Reduced X-ray resistance and homologous recombination frequencies in a RAD54(-/-) mutant of the chicken DT40 cell line [J].

Bezzubova, O ;

Silbergleit, A ;

YamaguchiIwai, Y ;

Takeda, S ;

Buerstedde, JM .

CELL, 1997, 89 (02) :185-193

[7] Xrcc3 is required for assembly of Rad51 complexes in vivo [J].

Bishop, DK ;

Ear, U ;

Bhattacharyya, A ;

Calderone, C ;

Beckett, M ;

Weichselbaum, RR ;

Shinohara, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (34) :21482-21488

[8] Cdc2-cyclin B kinase activity links Crb2 and Rqh1-topoisomerase III [J].

Caspari, T ;

Murray, JM ;

Carr, AM .

GENES & DEVELOPMENT, 2002, 16 (10) :1195-1208

[9] LOSS OF S-PHASE-DEPENDENT RADIORESISTANCE IN IRS-1 CELLS EXPOSED TO X-RAYS [J].

CHEONG, N ;

WANG, XM ;

WANG, Y ;

ILIAKIS, G .

MUTATION RESEARCH, 1994, 314 (01) :77-85

[10]

Dorée M, 2002, J CELL SCI, V115, P2461

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