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

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.

Pubmed ID: 21098477

Authors

  • Duch A
  • Palou G
  • Jonsson ZO
  • Palou R
  • Calvo E
  • Wohlschlegel J
  • Quintana DG

Journal

The Journal of biological chemistry

Publication Data

January 28, 2011

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM089778
  • Agency: NIGMS NIH HHS, Id: R01 GM089778

Mesh Terms

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