Published online 27 July 2004
Nucleic Acids Research, Vol. 32 No. 13 © Oxford University Press 2004; all rights reserved
SMC1 coordinates DNA double-strand break repair pathways
Institute of Biochemistry and Genetics, DKBW, University of Basel, CH-4058 Basel, Switzerland, 1 Institute of Molecular Cancer Research, University of Zürich, CH-8029 Zürich, Switzerland and 2 Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
* To whom correspondence should be addressed. Tel: +41 0 61 267 0767; Fax: +41 0 61 267 3566; Email: primo.schaer{at}unibas.ch
Received June 8, 2004; Revised and Accepted July 4, 2004
The SMC1/SMC3 heterodimer acts in sister chromatid cohesion, and recent data indicate a function in DNA double-strand break repair (DSBR). Since this role of SMC proteins has remained largely elusive, we explored interactions between SMC1 and the homologous recombination (HR) or non-homologous end-joining (NHEJ) pathways for DSBR in Saccharomyces cerevisiae. Analysis of conditional single- and double mutants of smc1-2 with rad52
, rad54, rad50 or dnl4 illustrates a significant contribution of SMC1 to the overall capacity of cells to repair DSBs. smc1 but not smc2 mutants show increased hypersensitivity of HR mutants to ionizing irradiation and to the DNA crosslinking agent cis-platin. Haploid, but not diploid smc1-2 mutants were severely affected in repairing multiple genomic DNA breaks, suggesting a selective role of SMC1 in sister chromatid recombination. smc1-2 mutants were also 15-fold less efficient and highly error-prone in plasmid end-joining through the NHEJ pathway. Strikingly, inactivation of RAD52 or RAD54 fully rescued efficiency and accuracy of NHEJ in the smc1 background. Therefore, we propose coordination of HR and NHEJ processes by Smc1p through interaction with the RAD52 pathway.
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