Checkpoint activation regulates mutagenic translesion synthesis

Mihoko Kai, Teresa S.F. Wang

Research output: Contribution to journalArticlepeer-review

140 Scopus citations


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 Polζ. 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.

Original languageEnglish (US)
Pages (from-to)64-76
Number of pages13
JournalGenes and Development
Issue number1
StatePublished - Jan 1 2003
Externally publishedYes


  • Cds1
  • Checkpoint response
  • DinB
  • Mutagenic translesion synthesis
  • Mutator phenotype
  • Rad17

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


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