Saccharomyces Ku70, Mre11/Rad50, and RPA proteins regulate adaptation to G2/M arrest after DNA damage

Sang Eun Lee, J. Kent Moore, Allyson Holmes, Keiko Umezu, Richard D. Kolodner, James E. Haber

Research output: Contribution to journalArticlepeer-review

607 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)399-409
Number of pages11
JournalCell
Volume94
Issue number3
DOIs
StatePublished - Aug 7 1998

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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