Access

You are not currently logged in.

Access JSTOR through your library or other institution:

login

Log in through your institution.

Journal Article

Mechanism of RAD51-Dependent DNA Interstrand Cross-Link Repair

David T. Long, Markus Räschle, Vladimir Joukov and Johannes C. Walter
Science
New Series, Vol. 333, No. 6038 (1 July 2011), pp. 84-87
Stable URL: http://www.jstor.org/stable/27978152
Page Count: 4

You can always find the topics here!

Topics: DNA, Eggs, Chromatids, Lesions, Plasmids, Gels, Nucleotides, Molecules, Cruciform DNA
Were these topics helpful?
See somethings inaccurate? Let us know!

Select the topics that are inaccurate.

Cancel
  • More info
  • Add to My Lists
  • Cite this Item
Preview not available
Preview not available

Abstract

DNA interstrand cross-links (ICLs) are toxic DNA lesions whose repair in S phase of eukaryotic cells is incompletely understood. In Xenopus egg extracts, ICL repair is initiated when two replication forks converge on the lesion. Dual incisions then create a DNA double-strand break (DSB) in one sister chromatid, whereas lesion bypass restores the other sister. We report that the broken sister chromatid is repaired via RAD51-dependent strand invasion into the regenerated sister. Recombination acts downstream of FANCI-FANCD2, yet RAD51 binds ICL-stalled replication forks independently of FANCI-FANCD2 and before DSB formation. Our results elucidate the functional link between the Fanconi anemia pathway and the recombination machinery during ICL repair. In addition, they demonstrate the complete repair of a DSB via homologous recombination in vitro.

Page Thumbnails

  • Thumbnail: Page 
84
    84
  • Thumbnail: Page 
85
    85
  • Thumbnail: Page 
86
    86
  • Thumbnail: Page 
87
    87