XPF-ERCC1 Acts in Unhooking DNA Interstrand Crosslinks in Cooperation with FANCD2 and FANCP/SLX4

被引：185

作者：

Douwel, Daisy Klein ^{[1
]}

Boonen, Rick A. C. M. ^{[1
]}

Long, David T. ^{[2
]}

Szypowska, Anna A. ^{[1
]}

Raschle, Markus ^{[3
]}

Walter, Johannes C. ^{[2
]}

Knipscheer, Puck ^{[1
]}

机构：

[1] Univ Med Ctr Utrecht, Hubrecht Inst KNAW, NL-3584 CT Utrecht, Netherlands

[2] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA

[3] Max Planck Inst Biochem, Dept Prote & Signal Transduct, D-82152 Martinsried, Germany

来源：

MOLECULAR CELL | 2014年 / 54卷 / 03期

基金：

美国国家卫生研究院;

关键词：

STRUCTURE-SPECIFIC NUCLEASES; HOLLIDAY JUNCTION RESOLVASE; FANCONI-ANEMIA; EXCISION-REPAIR; MOUSE SLX4; REPLICATION; MUTATIONS; ERCC1-XPF; PATHWAY; FAN1;

D O I：

10.1016/j.molcel.2014.03.015

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 interstrand crosslinks (ICLs), highly toxic lesions that covalently link the Watson and Crick strands of the double helix, are repaired by a complex, replication-coupled pathway in higher eukaryotes. The earliest DNA processing event in ICL repair is the incision of parental DNA on either side of the ICL ("unhooking''), which allows lesion bypass. Incisions depend critically on the Fanconi anemia pathway, whose activation involves ubiquitylation of the FANCD2 protein. Using Xenopus egg extracts, which support replication-coupled ICL repair, we show that the 30 flap endonuclease XPF-ERCC1 cooperates with SLX4/FANCP to carry out the unhooking incisions. Efficient recruitment of XPF-ERCC1 and SLX4 to the ICL depends on FANCD2 and its ubiquitylation. These data help define the molecular mechanism by which the Fanconi anemia pathway promotes a key event in replication-coupled ICL repair.

引用

页码：460 / 471

页数：12

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