| Literature DB >> 19595721 |
Ivan M Muñoz1, Karolina Hain, Anne-Cécile Déclais, Mary Gardiner, Geraldine W Toh, Luis Sanchez-Pulido, Johannes M Heuckmann, Rachel Toth, Thomas Macartney, Berina Eppink, Roland Kanaar, Chris P Ponting, David M J Lilley, John Rouse.
Abstract
Budding yeast Slx4 interacts with the structure-specific endonuclease Slx1 to ensure completion of ribosomal DNA replication. Slx4 also interacts with the Rad1-Rad10 endonuclease to control cleavage of 3' flaps during repair of double-strand breaks (DSBs). Here we describe the identification of human SLX4, a scaffold for DNA repair nucleases XPF-ERCC1, MUS81-EME1, and SLX1. SLX4 immunoprecipitates show SLX1-dependent nuclease activity toward Holliday junctions and MUS81-dependent activity toward other branched DNA structures. Furthermore, SLX4 enhances the nuclease activity of SLX1, MUS81, and XPF. Consistent with a role in processing recombination intermediates, cells depleted of SLX4 are hypersensitive to genotoxins that cause DSBs and show defects in the resolution of interstrand crosslink-induced DSBs. Depletion of SLX4 causes a decrease in DSB-induced homologous recombination. These data show that SLX4 is a regulator of structure-specific nucleases and that SLX4 and SLX1 are important regulators of genome stability in human cells.Entities:
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Year: 2009 PMID: 19595721 DOI: 10.1016/j.molcel.2009.06.020
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970