Reference - PMID:12514100 - Checkpoint activation regulates mutagenic translesion synthesis.

Reference summary

PubMed ID

PMID:12514100

Title

Checkpoint activation regulates mutagenic translesion synthesis.

Authors

Kai M, Wang TS

Citation

Genes Dev 2003 Jan 01;17(1):64-76

Publication year

2003

Abstract

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.

Annotation