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To preserve genome integrity, the S-phase checkpoint senses damaged DNA or nucleotide depletion and when necessary, arrests replication progression and delays cell division. Previous studies, based on two  pol2  mutants have suggested the involvement of DNA polymerase epsilon (Pol ε) in sensing DNA replication accuracy in  Saccharomyces cerevisiae . Here we have studied the involvement of Pol ε in sensing proper progression of DNA replication, using a mutant in  DPB2 , the gene coding for a non-catalytic subunit of Pol ε. Under genotoxic conditions, the  dpb2-103  cells progress through S phase faster than wild-type cells. Moreover, the Nrm1-dependent branch of the checkpoint, which regulates the expression of many replication checkpoint genes, is impaired in  dpb2-103  cells. Finally, deletion of  DDC1  in the  dpb2-103  mutant is lethal supporting a model of strand-specific activation of the replication checkpoint. This lethality is suppressed by  NRM1  deletion. We postulate that improper activation of the Nrm1-branch may explain inefficient replication checkpoint activation in Pol ε mutants.

Mutations in the Non-Catalytic Subunit Dpb2 of DNA Polymerase Epsilon Affect the Nrm1 Branch of the DNA Replication Checkpoint