The Mre11 Complex and ATM: Collaborating to Navigate S Phase

Curr Opin Cell Biol. 2000 Jun;12(3):293-6. doi: 10.1016/s0955-0674(00)00091-0.


Recently, findings regarding a group of cancer predisposition and chromosome instability syndromes, Nijmegen breakage syndrome (NBS), the ataxia-telangiectasia-like disorder (A-TLD) and ataxia telangiectasia have shed light on the unexpected role of recombinational DNA repair proteins in DNA-damage-dependent cell-cycle regulation. Mutations in the Mre11 complex cause A-TLD and NBS. In addition, functions of the Mre11 complex have been biochemically linked to ATM, the large protein kinase that is defective in ataxia-telangiectasia cells by the observation that Nbs1 is a bona fide substrate of the ATM kinase.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Ataxia Telangiectasia / genetics
  • Ataxia Telangiectasia / metabolism
  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins
  • DNA Damage
  • DNA Repair
  • DNA Replication
  • DNA-Binding Proteins
  • Endodeoxyribonucleases*
  • Exodeoxyribonucleases*
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism*
  • Humans
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Serine-Threonine Kinases / metabolism*
  • Recombination, Genetic
  • S Phase / genetics
  • S Phase / physiology*
  • Saccharomyces cerevisiae Proteins*
  • Tumor Suppressor Proteins


  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Fungal Proteins
  • Saccharomyces cerevisiae Proteins
  • Tumor Suppressor Proteins
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein-Serine-Threonine Kinases
  • Endodeoxyribonucleases
  • Exodeoxyribonucleases
  • MRE11 protein, S cerevisiae