The Mre11 complex and ATM: collaborating to navigate S phase

Recently, findings regarding a group of cancer predisposition and chromosom e instability syndromes, Nijmegen breakage syndrome (NBS), the ataxia-telan giectasia-like disorder (A-TLD) and ataxia telangiectasia have shed light o n 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 biochemical ly linked to ATM, the large protein kinase that is defective in ataxia-tela ngiectasia cells by the observation that Nbs1 is a bona fide substrate of t he ATM kinase.