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A DNA damage response pathway controlled by Tel1 and the Mre11 complex.

We define a DNA damage checkpoint pathway in S. cerevisiae governed by the ATM homolog Tel1 and the Mre11 complex. In mitotic cells, the Tel1-Mre11 complex pathway triggers Rad53 activation and its interaction with Rad9, whereas in meiosis it acts via Rad9 and the Rad53 paralog Mre4/Mek1. Activation of the Tel1-Mre11 complex pathway checkpoint functions appears to depend upon the Mre11 complex as a damage sensor and, at least in meiotic cells, to depend on unprocessed DNA double-strand breaks (DSBs). The DSB repair functions of the Mre11 complex are enhanced by the pathway, suggesting that the complex both initiates and is regulated by the Tel1-dependent DSB signal. These findings demonstrate that the diverse functions of the Mre11 complex in the cellular DNA damage response are conserved in mammals and yeast.

Pubmed ID: 11430828

Authors

  • Usui T
  • Ogawa H
  • Petrini JH

Journal

Molecular cell

Publication Data

June 29, 2001

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM56888

Mesh Terms

  • Cell Cycle Proteins
  • Checkpoint Kinase 2
  • DNA Damage
  • DNA Repair
  • DNA-Binding Proteins
  • Endodeoxyribonucleases
  • Exodeoxyribonucleases
  • Fungal Proteins
  • Genes, cdc
  • Intracellular Signaling Peptides and Proteins
  • Protein Kinases
  • Protein-Serine-Threonine Kinases
  • Saccharomyces cerevisiae Proteins
  • Yeasts