Checkpoint activation regulates mutagenic translesion synthesis.
Cells have evolved checkpoint responses to arrest or delay the cell cycle, activate DNA repair networks, or induce apoptosis after genomic perturbation. Cells have also evolved the translesion synthesis processes to tolerate genomic lesions by either error-free or error-prone repair. Here, we show that after a replication perturbation, cells exhibit ... a mutator phenotype, which can be significantly affected by mutations in the checkpoint elements Cds1 and Rad17 or translesion synthesis polymerases DinB and Polzeta. Cells respond to genomic perturbation by up-regulation of DinB in a checkpoint activation-dependent manner. Moreover, association of DinB with chromatin is dependent on functional Rad17, and DinB physically interacts with the checkpoint-clamp components Hus1 and Rad1. Thus, translesion synthesis is a part of the checkpoint response.
Mesh Terms:
Bacterial Proteins, Cell Cycle, Cell Cycle Proteins, Chromatin, DNA Polymerase I, DNA Repair, DNA Repair Enzymes, DNA Replication, DNA-Binding Proteins, DNA-Directed DNA Polymerase, Endonucleases, Escherichia coli Proteins, Genes, cdc, Mutagenesis, Nuclear Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Schizosaccharomyces pombe Proteins
Bacterial Proteins, Cell Cycle, Cell Cycle Proteins, Chromatin, DNA Polymerase I, DNA Repair, DNA Repair Enzymes, DNA Replication, DNA-Binding Proteins, DNA-Directed DNA Polymerase, Endonucleases, Escherichia coli Proteins, Genes, cdc, Mutagenesis, Nuclear Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Schizosaccharomyces pombe Proteins
Genes Dev.
Date: Jan. 01, 2003
PubMed ID: 12514100
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