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

Nat Cell Biol. 2006 Sep;8(9):1032-4. doi: 10.1038/ncb1466. Epub 2006 Aug 6.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Proteins / physiology*
  • DNA / metabolism
  • DNA Damage*
  • Deoxyribonucleases, Type II Site-Specific / metabolism
  • Genomic Instability
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / physiology*
  • Saccharomyces cerevisiae Proteins / physiology*
  • Sister Chromatid Exchange*


  • Cell Cycle Proteins
  • SMC5 protein, S cerevisiae
  • SMC6 protein, S cerevisiae
  • Saccharomyces cerevisiae Proteins
  • DNA
  • SCEI protein, S cerevisiae
  • Deoxyribonucleases, Type II Site-Specific