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

http://www.ncbi.nlm.nih.gov/pubmed/21098477

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 RIS Download

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

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Associated grants

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

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