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Author:
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De Piccoli, Giacomo; Cortes Ledesma, Felipe; Ira, Gregory; Torres Rosell, Jordi; Uhle, Stefan; Farmer, Sarah; Hwang, Ji-Young; Machín, Félix; Ceschia, Audrey; McAleenan, Alexandra; Cordon Preciado, Violeta; Clemente Blanco, Andrés; Vilella Mitjana, Felipe; Ullal, Pranav; Jarmuz, Adam; Leitao, Beatriz; Bressan, Debra; Dotiwala, Farokh; Papusha, Alma; Zhao, Xiaolan; Myung, Kyungjae; Haber, James E.; Aguilera, Andrés; Aragón, Luis
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Notes:
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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 sisterchromatid
recombination (SCR), thereby suppressing
inappropriate non-sister recombination events.
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. |
