Mechanism of replication-coupled DNA interstrand crosslink repair

被引：400

作者：

Raeschle, Markus ^{[1
]}

Knipscheer, Puck ^{[1
]}

Enoiu, Milica ^{[2
]}

Angelov, Todor ^{[2
]}

Sun, Jingchuan ^{[3
]}

Griffith, Jack D. ^{[3
]}

Ellenberger, Tom E. ^{[4
]}

Schaerer, Orlando D. ^{[2
,5
]}

Walter, Johannes C. ^{[1
]}

机构：

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

[2] Univ Zurich, Inst Mol Canc Res, CH-8057 Zurich, Switzerland

[3] Univ N Carolina, Lineberger Canc Ctr, Chapel Hill, NC 27599 USA

[4] Washington Univ, Dept Biochem & Mol Biophys, St Louis, MO 63110 USA

[5] SUNY Stony Brook, Dept Pharmacol Sci, Stony Brook, NY 11794 USA

来源：

CELL | 2008年 / 134卷 / 06期

关键词：

D O I：

10.1016/j.cell.2008.08.030

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) are toxic DNA lesions whose repair occurs in the S phase of metazoans via an unknown mechanism. Here, we describe a cell-free system based on Xenopus egg extracts that supports ICL repair. During DNA replication of a plasmid containing a site-specific ICL, two replication forks converge on the crosslink. Subsequent lesion bypass involves advance of a nascent leading strand to within one nucleotide of the ICL, followed by incisions, translesion DNA synthesis, and extension of the nascent strand beyond the lesion. Immunodepletion experiments suggest that extension requires DNA polymerase zeta. Ultimately, a significant portion of the input DNA is fully repaired, but not if DNA replication is blocked. Our experiments establish a mechanism for ICL repair that reveals how this process is coupled to DNA replication.

引用

页码：969 / 980

页数：12

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