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

Alba Duch, Gloria Palou, Zophonias O. Jonsson, Roger Palou, Enrique Calvo, James Wohlschlegel, David G. Quintana

Research output: Contribution to journalArticleResearchpeer-review

22 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2486-2491
Number of pages6
JournalJournal of Biological Chemistry
Volume286
Issue number4
DOIs
Publication statusPublished - 28 Jan 2011

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