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Replication Checkpoint: Tuning and Coordination of Replication Forks in S Phase

Overview
Journal Genes (Basel)
Publisher MDPI
Date 2014 Apr 8
PMID 24705211
Citations 38
Authors
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Abstract

Checkpoints monitor critical cell cycle events such as chromosome duplication and segregation. They are highly conserved mechanisms that prevent progression into the next phase of the cell cycle when cells are unable to accomplish the previous event properly. During S phase, cells also provide a surveillance mechanism called the DNA replication checkpoint, which consists of a conserved kinase cascade that is provoked by insults that block or slow down replication forks. The DNA replication checkpoint is crucial for maintaining genome stability, because replication forks become vulnerable to collapse when they encounter obstacles such as nucleotide adducts, nicks, RNA-DNA hybrids, or stable protein-DNA complexes. These can be exogenously induced or can arise from endogenous cellular activity. Here, we summarize the initiation and transduction of the replication checkpoint as well as its targets, which coordinate cell cycle events and DNA replication fork stability.

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References
1.
Shimada K, Pasero P, Gasser S . ORC and the intra-S-phase checkpoint: a threshold regulates Rad53p activation in S phase. Genes Dev. 2002; 16(24):3236-52. PMC: 187497. DOI: 10.1101/gad.239802. View

2.
Patro B, Frohlich R, Bohr V, Stevnsner T . WRN helicase regulates the ATR-CHK1-induced S-phase checkpoint pathway in response to topoisomerase-I-DNA covalent complexes. J Cell Sci. 2011; 124(Pt 23):3967-79. PMC: 3244981. DOI: 10.1242/jcs.081372. View

3.
Osborn A, Elledge S . Mrc1 is a replication fork component whose phosphorylation in response to DNA replication stress activates Rad53. Genes Dev. 2003; 17(14):1755-67. PMC: 196183. DOI: 10.1101/gad.1098303. View

4.
Morrison A, Kim J, Person M, Highland J, Xiao J, Wehr T . Mec1/Tel1 phosphorylation of the INO80 chromatin remodeling complex influences DNA damage checkpoint responses. Cell. 2007; 130(3):499-511. DOI: 10.1016/j.cell.2007.06.010. View

5.
Sun Z, Hsiao J, Fay D, Stern D . Rad53 FHA domain associated with phosphorylated Rad9 in the DNA damage checkpoint. Science. 1998; 281(5374):272-4. DOI: 10.1126/science.281.5374.272. View