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Smc5–Smc6 mediate DNA double-strand-break repair by promoting sister-chromatid recombination

Nature Cell Biology volume 8, pages 1032–1034 (2006)Cite this article

Abstract

DNA double-strand breaks (DSB) can arise during DNA replication, or after exposure to DNA-damaging agents, and their correct repair is fundamental for cell survival and genomic stability. Here, we show that the Smc5–Smc6 complex is recruited to DSBs de novo to support their repair by homologous recombination between sister chromatids. In addition, we demonstrate that Smc5–Smc6 is necessary to suppress gross chromosomal rearrangements. Our findings show that the Smc5–Smc6 complex is essential for genome stability as it promotes repair of DSBs by error-free sister-chromatid recombination (SCR), thereby suppressing inappropriate non-sister recombination events.

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Figure 1: The Smc5–Smc6 complex is enriched around a HO-induced DSB during G2–M.
Figure 2: Inactivation of Smc5–Smc6 reduces DSB repair by SCR.

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Acknowledgements

We would like to thank H. Yu, R. Potts and C. Sjogren for communicating results before publication. The Medical Research Council UK supported the Aragón laboratory. The Ministerio de Educación y Ciencia, Spain (grant SAF2003-00204) funded work in the Aguilera laboratory. Funding for the Haber laboratory is from the National Institutes of Health (NIH; grant GM20056). F.C.-L. is a fellow from the Fondo de Investigaciones Sanitarias, Spain. G.I. is a Charles A. King Medical Foundation of Boston fellow. S.U. is a Marie Curie Fellow from the EU.

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Author notes

  1. Jordi Torres-Rosell

    Present address: Dept. Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida, Montserrat Roig, 2, 25008, Lleida, Spain

  2. Giacomo De Piccoli, Felipe Cortes-Ledesma and Gregory Ira: These authors contributed equally to this work.

Authors and Affiliations

  1. Cell Cycle Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London, W12 0NN, UK

    Giacomo De Piccoli, Jordi Torres-Rosell, Stefan Uhle, Sarah Farmer, Felix Machin, Audrey Ceschia, Alexandra McAleenan, Violeta Cordon-Preciado, Andrés Clemente-Blanco, Felip Vilella-Mitjana, Pranav Ullal, Adam Jarmuz, Beatriz Leitao & Luis Aragón

  2. Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Sevilla, 41012, Spain

    Felipe Cortes-Ledesma & Andrés Aguilera

  3. Rosenstiel Center, Brandeis University, 415 South St., Mail Stop 029, Waltham, 02454–9110, MA, USA

    Gregory Ira, Debra Bressan, Farokh Dotiwala & James E. Haber

  4. Department of Human and Molecular Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA

    Gregory Ira & Alma Papusha

  5. Genome Instability Section, Genetics & Molecular Biology Branch, National Human Genome Research Institute, NIH, 49 Convent Drive, Bethesda, 20892–4442, MD, USA

    Ji-Young Hwang & Kyungjae Myung

  6. Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, 10021, NY, USA

    Xiaolan Zhao

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  1. Giacomo De Piccoli
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Correspondence to James E. Haber, Andrés Aguilera or Luis Aragón.

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Supplementary Figures S1, S2 and Supplementary Materials (PDF 2272 kb)

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De Piccoli, G., Cortes-Ledesma, F., Ira, G. et al. Smc5–Smc6 mediate DNA double-strand-break repair by promoting sister-chromatid recombination. Nat Cell Biol 8, 1032–1034 (2006). https://doi.org/10.1038/ncb1466

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