Mechanism of DNA interstrand cross-link processing by repair nuclease FAN1

被引：53

作者：

Wang, Renjing ^{[1
,2
]}

Persky, Nicole S. ^{[1
,2
]}

Yoo, Barney ^{[3
]}

Ouerfelli, Ouathek ^{[3
]}

Smogorzewska, Agata ^{[4
]}

Elledge, Stephen J. ^{[5
,6
,7
]}

Pavletich, Nikola P. ^{[1
,2
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Struct Biol Program, New York, NY 10065 USA

[2] Mem Sloan Kettering Canc Ctr, Howard Hughes Med Inst, New York, NY 10065 USA

[3] Mem Sloan Kettering Canc Ctr, Mol Pharmacol & Chem Program, New York, NY 10065 USA

[4] Rockefeller Univ, Lab Genome Maintenance, New York, NY 10065 USA

[5] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA

[6] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA

[7] Brigham & Womens Hosp, Div Genet, Boston, MA 02115 USA

来源：

SCIENCE | 2014年 / 346卷 / 6213期

关键词：

KIAA1018/FAN1; CELLS; IDENTIFICATION; DAMAGE;

D O I：

10.1126/science.1258973

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 interstrand cross-links (ICLs) are highly toxic lesions associated with cancer and degenerative diseases. ICLs can be repaired by the Fanconi anemia (FA) pathway and through FA-independent processes involving the FAN1 nuclease. In this work, FAN1-DNA crystal structures and biochemical data reveal that human FAN1 cleaves DNA successively at every third nucleotide. In vitro, this exonuclease mechanism allows FAN1 to excise an ICL from one strand through flanking incisions. DNA access requires a 5 '-terminal phosphate anchor at a nick or a 1- or 2-nucleotide flap and is augmented by a 3 ' flap, suggesting that FAN1 action is coupled to DNA synthesis or recombination. FAN1 ' s mechanism of ICL excision is well suited for processing other localized DNA adducts as well.

引用

页码：1127 / 1130

页数：4

共 20 条

[1] Advances in Understanding the Complex Mechanisms of DNA Interstrand Cross-Link Repair [J].

Clauson, Cheryl ;

Schaerer, Orlando D. ;

Niedernhofer, Laura .

COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, 2013, 5 (10)

[2] DNA interstrand crosslink repair and cancer [J].

Deans, Andrew J. ;

West, Stephen C. .

NATURE REVIEWS CANCER, 2011, 11 (07) :467-480

[3] The conserved Fanconi anemia nuclease Fan1 and the SUMO E3 ligase Pli1 act in two novel Pso2-independent pathways of DNA interstrand crosslink repair in yeast [J].

Fontebasso, Y. ;

Etheridge, T. J. ;

Oliver, A. W. ;

Murray, J. M. ;

Carr, A. M. .

DNA REPAIR, 2013, 12 (12) :1011-1023

[4] The structural basis of Holliday junction resolution by T7 endonuclease [J].

Hadden, Jonathan M. ;

Declais, Anne-Cecile ;

Carr, Stephen B. ;

Lilley, David M. J. ;

Phillips, Simon E. V. .

NATURE, 2007, 449 (7162) :621-U15

[5] Regulation of DNA cross-link repair by the Fanconi anemia/BRCA pathway [J].

Kim, Hyungjin ;

D'Andrea, Alan D. .

GENES & DEVELOPMENT, 2012, 26 (13) :1393-1408

[6] Identification of novel restriction endonuclease-like fold families among hypothetical proteins [J].

Kinch, LN ;

Ginalski, K ;

Rychlewski, L ;

Grishin, NV .

NUCLEIC ACIDS RESEARCH, 2005, 33 (11) :3598-3605

[7] Deficiency of FANCD2-Associated Nuclease KIAA1018/FAN1 Sensitizes Cells to Interstrand Crosslinking Agents [J].

Kratz, Katja ;

Schoepf, Barbara ;

Kaden, Svenja ;

Sendoel, Ataman ;

Eberhard, Ralf ;

Lademann, Claudio ;

Cannavo, Elda ;

Sartori, Alessandro A. ;

Hengartner, Michael O. ;

Jiricny, Josef .

CELL, 2010, 142 (01) :77-88

[8] FAN1 Acts with FANCI-FANCD2 to Promote DNA Interstrand Cross-Link Repair [J].

Liu, Ting ;

Ghosal, Gargi ;

Yuan, Jingsong ;

Chen, Junjie ;

Huang, Jun .

SCIENCE, 2010, 329 (5992) :693-696

[9] Mechanism of RAD51-Dependent DNA Interstrand Cross-Link Repair [J].

Long, David T. ;

Raeschle, Markus ;

Joukov, Vladimir ;

Walter, Johannes C. .

SCIENCE, 2011, 333 (6038) :84-87

[10] Identification of KIAA1018/FAN1, a DNA Repair Nuclease Recruited to DNA Damage by Monoubiquitinated FANCD2 [J].

MacKay, Craig ;

Declais, Anne-Cecile ;

Lundin, Cecilia ;

Agostinho, Ana ;

Deans, Andrew J. ;

MacArtney, Thomas J. ;

Hofmann, Kay ;

Gartner, Anton ;

West, Stephen C. ;

Helleday, Thomas ;

Lilley, David M. J. ;

Rouse, John .

CELL, 2010, 142 (01) :65-76

← 1 2 →