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      Saccharomyces Ku70, mre11/rad50 and RPA proteins regulate adaptation to G2/M arrest after DNA damage.

      1 , , , , ,
      Cell
      Elsevier BV

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          Abstract

          Saccharomyces cells suffering a single unrepairable double-strand break (DSB) exhibit a long, but transient arrest at G2/M. hdf1 cells, lacking Ku70p, fail to escape from this RAD9/RAD17-dependent checkpoint. The effect of hdf1 results from its accelerated 5' to 3' degradation of the broken chromosome. Permanent arrest in hdf1 cells is suppressed by rad50 or mre11 deletions that retard this degradation. Wild-type HDF1 cells also become permanently arrested when they experience two unrepairable DSBs. Both DSB-induced arrest conditions are suppressed by a mutation in the single-strand binding protein, RPA. We suggest that escape from the DNA damage-induced G2/M checkpoint depends on the extent of ssDNA created at broken chromosome ends. RPA appears to play a key intermediate step in this adaptation.

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          Author and article information

          Journal
          Cell
          Cell
          Elsevier BV
          0092-8674
          0092-8674
          Aug 07 1998
          : 94
          : 3
          Affiliations
          [1 ] Rosenstiel Center, Department of Biology, Brandeis University, Waltham, Massachusetts 02454-9110, USA.
          Article
          S0092-8674(00)81482-8
          10.1016/s0092-8674(00)81482-8
          9708741
          97276ba0-1744-419d-a669-a3d62dea8844
          History

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