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Sci. Signal., 5 July 2011
Vol. 4, Issue 180, p. ec187
[DOI: 10.1126/scisignal.4180ec187]

EDITORS' CHOICE

DNA Repair Damage Limitation Exercise

Guy Riddihough

Science, AAAS, Washington, DC 20005, USA

Covalent interstrand cross-links (ICLs) in the genome must be repaired quickly to avoid disruption of DNA-based cellular processes and additional damage to the DNA. Vertebrates can repair ICLs during DNA replication in a process that involves Fanconi anemia (FA) proteins and is also thought to require homologous recombination between sister chromatids. Long et al. used a Xenopus egg-based cell-free system to show that in replication-coupled ICL repair, Rad51 is required for homologous recombination of the double-strand break in the incised sister chromatid. Rad51 is loaded onto stalled replication forks before double-strand break formation, likely functioning to initiate strand invasion as soon as the break occurs. The FA protein complex acts upstream of homologous recombination during interstrand cross-link repair and is not required for Rad51 recruitment to chromatin.

D. T. Long, M. Räschle, V. Joukov, J. C. Walter, Mechanism of RAD51-dependent DNA interstrand cross-link repair. Science 333, 84–87 (2011). [Abstract] [Full Text]

Citation: G. Riddihough, Damage Limitation Exercise. Sci. Signal. 4, ec187 (2011).

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