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Novel insights into the roles of Cdc7 in response to replication stress
Author(s) -
GonzálezGarrido Cristina,
Prado Félix
Publication year - 2023
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.16456
Subject(s) - minichromosome maintenance , origin recognition complex , control of chromosome duplication , dna replication , microbiology and biotechnology , replication (statistics) , replication factor c , biology , pre replication complex , dna replication factor cdt1 , origin of replication , dna damage , eukaryotic dna replication , dna re replication , licensing factor , dna , genetics , virology
Cdc7 and its regulator Dbf4 (Dbf4‐dependent kinase; DDK) form an essential complex due to its function in replication initiation, which is carried out by phosphorylating different residues at the helicase MCM during the G1/S transition. In response to replication stress, late origins are inhibited to prevent cell cycle progression until the problems are resolved. In yeast, this inhibition is partially achieved by attenuating DDK activity. In addition, evidence from yeast to human shows that Cdc7 is required for a successful DNA damage response by coordinating multiple processes dealing with replication stress (replication checkpoint, DNA damage tolerance and break‐induced replication) through mechanisms that go beyond its role in origin activation. These studies reveal the importance of getting a better understanding of the spatiotemporal regulation of DDK. Here, we will discuss how DDK operates in these processes and its putative role in controlling the activity of replication and repair factors at specific nuclease‐resistant nucleoprotein scaffolds.