Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication

被引：72

作者：

Shen, Xi ^{[1
]}

Do, Huong ^{[1
]}

Li, Yongjiang ^{[3
]}

Chung, Woo-Hyun ^{[1
]}

Tomasz, Maria ^{[4
]}

de Winter, Johan P. ^{[5
]}

Xia, Bing ^{[6
]}

Elledge, Stephen J. ^{[7
]}

Wang, Weidong ^{[3
]}

Li, Lei ^{[1
,2
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Expt Radiat Oncol, Houston, TX 77030 USA

[2] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA

[3] NIA, Genet Lab, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA

[4] CUNY Hunter Coll, Dept Chem, New York, NY 10021 USA

[5] Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, NL-1081 BT Amsterdam, Netherlands

[6] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Radiat Oncol, Canc Inst New Jersey, New Brunswick, NJ 08903 USA

[7] Harvard Univ, Sch Med, Harvard Partners Ctr Genet & Genom, Howard Hughes Med Inst,Dept Genet, Boston, MA 02115 USA

来源：

MOLECULAR CELL | 2009年 / 35卷 / 05期

关键词：

EPSTEIN-BARR-VIRUS; NUCLEOTIDE EXCISION-REPAIR; INTERSTRAND CROSS-LINKS; ORIGIN-BINDING-PROTEIN; HOMOLOGOUS RECOMBINATION; CORE COMPLEX; FANCD2; BRCA2; SUSCEPTIBILITY; PATHWAY;

D O I：

10.1016/j.molcel.2009.06.034

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：

Fanconi anemia (FA) is characterized by cellular hypersensitivity to DNA crosslinking agents, but how the Fanconi pathway protects cells from DNA crosslinks and whether FA proteins act directly on crosslinks remain unclear. We developed a chromatin-IP-based strategy termed eChIP and detected association of multiple FA proteins with DNA crosslinks in vivo. Interdependence analyses revealed that crosslink-specific enrichment of various FA proteins is controlled by distinct mechanisms. BRCA-related FA proteins (BRCA2, FANCJ/BACH1, and FANCN/PALB2), but not FA core and I/D2 complexes, require replication for their crosslink association. FANCD2, but not FANCJ and FANCN, requires the FA core complex for its recruitment. FA core complex requires nucleotide excision repair proteins XPA and XPC for its association. Consistent with the distinct recruitment mechanism, recombination-independent crosslink repair was inversely affected in cells deficient of FANC-core versus BRCA-related FA proteins. Thus, FA proteins participate in distinct DNA damage response mechanisms governed by DNA replication status.

引用

页码：716 / 723

页数：8

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