A Dbf4 mutant contributes to bypassing the Rad53-mediated block of origins of replication in response to genotoxic stress

J Biol Chem. 2011 Jan 28;286(4):2486-91. doi: 10.1074/jbc.M110.190843. Epub 2010 Nov 23.

Abstract

An intra-S phase checkpoint slows the rate of DNA replication in response to DNA damage and replication fork blocks in eukaryotic cells. In the budding yeast Saccharomyces cerevisiae, such down-regulation is achieved through the Rad53 kinase-dependent block of origins of replication. We have identified the Rad53 phosphorylation sites on Dbf4, the activator subunit of the essential S phase Dbf4-dependent kinase, and generated a non-phosphorylatable Dbf4 mutant (dbf4(7A)). We show here that dbf4(7A) is a bona fide intra-S phase checkpoint bypass allele that contributes to abrogating the Rad53 block of origin firing in response to genotoxic stress.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism*
  • Checkpoint Kinase 2
  • DNA Damage*
  • DNA, Fungal / genetics
  • DNA, Fungal / metabolism*
  • Mutation
  • Phosphorylation / genetics
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Replication Origin
  • S Phase*
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / metabolism*
  • Saccharomyces cerevisiae Proteins / genetics
  • Saccharomyces cerevisiae Proteins / metabolism*

Substances

  • Cell Cycle Proteins
  • DNA, Fungal
  • Dbf4 protein, S cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Checkpoint Kinase 2
  • Protein Serine-Threonine Kinases
  • RAD53 protein, S cerevisiae