Origin Association of Sld3, Sld7, and Cdc45 Proteins Is a Key Step for Determination of Origin-Firing Timing

Tanaka, Seiji; Nakato, Ryuichiro; Katou, Yuki; Shirahige, Katsuhiko; Araki, Hideki

doi:10.1016/j.cub.2011.11.038

Cited by 243 publications

(321 citation statements)

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“…2A). DDK activity is generally low during G1 due to low Dbf4 levels (Oshiro et al 1999;Weinreich and Stillman 1999;Ferreira et al 2000), although the presence of some functional DDK during G1 phase has been demonstrated (Katou et al 2006;Tanaka et al 2011). The increase in Mcm4 phosphorylation caused by deleting Rif1 was not due to increased or precocious Dbf4 expression, as Western analysis revealed no change in Dbf4 levels in the rif1D mutant in either S phase (Supplemental Fig.…”

Section: Rif1 Suppresses Mcm4 Phosphorylationmentioning

confidence: 99%

“…A previous study of the S. cerevisiae rif1D replication program showed a shortened interval between replication of early and late sequences, with telomeric origins in particular replicating aberrantly early (Lian et al 2011). Loss of Rif1-mediated targeting of PP1 to dephosphorylate Mcm4 could conceivably cause a derailed replication program, since the level of DDK-mediated MCM phosphorylation is one of the factors likely to affect the initiation time of specific origins (Mantiero et al 2011;Tanaka et al 2011).…”

Section: Backup S-phase Controls and Regulation Of Replication Timingmentioning

confidence: 99%

“…Dbf4 levels are controlled by cell cycleregulated transcription and destruction and peak during S phase (Oshiro et al 1999;Weinreich and Stillman 1999;Ferreira et al 2000). Despite this tight cell cycle control, a low level of DDK activity exists during G1 phase, and Dbf4 protein is recruited to early origins (Katou et al 2006;Tanaka et al 2011). Preferential recruitment of Dbf4 may therefore be one of the key steps defining early origins.…”

mentioning

confidence: 99%

“…In the budding yeast Saccharomyces cerevisiae, DDK is composed of the catalytic subunit Cdc7 and its activator, Dbf4. Dbf4 is one of the factors that limits replication initiation and so plays a role in execution of the replication timing program (Mantiero et al 2011;Tanaka et al 2011). Dbf4 levels are controlled by cell cycleregulated transcription and destruction and peak during S phase (Oshiro et al 1999;Weinreich and Stillman 1999;Ferreira et al 2000).…”

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confidence: 99%

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Rif1 controls DNA replication by directing Protein Phosphatase 1 to reverse Cdc7-mediated phosphorylation of the MCM complex

et al. 2014

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Initiation of eukaryotic DNA replication requires phosphorylation of the MCM complex by Dbf4-dependent kinase (DDK), composed of Cdc7 kinase and its activator, Dbf4. We report here that budding yeast Rif1 (Rap1-interacting factor 1) controls DNA replication genome-wide and describe how Rif1 opposes DDK function by directing Protein Phosphatase 1 (PP1)-mediated dephosphorylation of the MCM complex. Deleting RIF1 partially compensates for the limited DDK activity in a cdc7-1 mutant strain by allowing increased, premature phosphorylation of Mcm4. PP1 interaction motifs within the Rif1 N-terminal domain are critical for its repressive effect on replication. We confirm that Rif1 interacts with PP1 and that PP1 prevents premature Mcm4 phosphorylation. Remarkably, our results suggest that replication repression by Rif1 is itself also DDK-regulated through phosphorylation near the PP1-interacting motifs. Based on our findings, we propose that Rif1 is a novel PP1 substrate targeting subunit that counteracts DDK-mediated phosphorylation during replication. Fission yeast and mammalian Rif1 proteins have also been implicated in regulating DNA replication. Since PP1 interaction sites are evolutionarily conserved within the Rif1 sequence, it is likely that replication control by Rif1 through PP1 is a conserved mechanism.

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Section: Rif1 Suppresses Mcm4 Phosphorylationmentioning

confidence: 99%

Section: Backup S-phase Controls and Regulation Of Replication Timingmentioning

confidence: 99%

mentioning

confidence: 99%

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Rif1 controls DNA replication by directing Protein Phosphatase 1 to reverse Cdc7-mediated phosphorylation of the MCM complex

et al. 2014

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“…DDK phosphorylates Mcm2 -7 Stillman 2006, 2010;Randell et al 2010). As a result of Mcm2 -7 phosphorylation, Cdc45 associates with Mcm2 -7 (Heller et al 2011;Tanaka et al 2011). Interestingly, this event occurs at a subset of origins before entry into S phase (Aparicio et al 1999;Kanemaki and Labib 2006;Heller et al 2011;Tanaka et al 2011).…”

Section: A Model For Helicase Loadingmentioning

confidence: 99%

Helicase Loading at Chromosomal Origins of Replication

Bell

Kaguni

2013

Cold Spring Harbor Perspectives in Biology

119

109

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Loading of the replicative DNA helicase at origins of replication is of central importance in DNA replication. As the first of the replication fork proteins assemble at chromosomal origins of replication, the loaded helicase is required for the recruitment of the rest of the replication machinery. In this work, we review the current knowledge of helicase loading at Escherichia coli and eukaryotic origins of replication. In each case, this process requires both an origin recognition protein as well as one or more additional proteins. Comparison of these events shows intriguing similarities that suggest a similar underlying mechanism, as well as critical differences that likely reflect the distinct processes that regulate helicase loading in bacterial and eukaryotic cells.

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Replication fork pausing at protein barriers on chromosomes

Hizume

Araki

2019

FEBS Letters

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When a cell divides prior to completion of DNA replication, serious DNA damage may occur. Thus, in addition to accuracy, the processivity of the replication forks is important. DNA synthesis at replication forks should be completed in time, and forks overcome aberrant structures on the template DNA, including damaged sites, using trans‐lesion synthesis, occasionally introducing mutations. By contrast, the protein barrier built on the DNA is known to block the progression of replication forks at specific chromosomal loci. Such protein barriers avert any collision of replication and transcription machineries, or control the recombination of specific loci. The components and the mechanisms of action of protein barriers have been revealed mainly using genetic and biochemical techniques. In addition to proteins involved in replication fork pausing, the interaction of the replicative helicase and DNA polymerase is also essential for replication fork pausing. Here, we provide an overview of replication fork pausing at protein barriers.

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Origin Association of Sld3, Sld7, and Cdc45 Proteins Is a Key Step for Determination of Origin-Firing Timing

Abstract: The DDK-dependent limited association between origins and Sld3-Sld7-Cdc45 is a key step for determining the timing of origin firing.

Cited by 243 publications

References 32 publications

Rif1 controls DNA replication by directing Protein Phosphatase 1 to reverse Cdc7-mediated phosphorylation of the MCM complex

Rif1 controls DNA replication by directing Protein Phosphatase 1 to reverse Cdc7-mediated phosphorylation of the MCM complex

Helicase Loading at Chromosomal Origins of Replication

Replication fork pausing at protein barriers on chromosomes

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