ArticleMolecular and cellular biology2004
Diminished S-phase cyclin-dependent kinase function elicits vital Rad53-dependent checkpoint responses in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Rpd3 regulates single-copy origins independently of the rDNA array by opposing Fkh1-mediated origin stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- A Mad2-Mediated Translational Regulatory Mechanism Promoting S-Phase Cyclin Synthesis Controls Origin Firing and Survival to Replication Stress.Molecular cell · 2018Article
- Sequential replication-coupled destruction at G1/S ensures genome stability.Genes & development · 2015Article
- Genetic Regulation of Dna2 Localization During the DNA Damage Response.G3 (Bethesda, Md.) · 2015Article
- Rif1 regulates initiation timing of late replication origins throughout the S. cerevisiae genome.PloS one · 2014Article
- The level of origin firing inversely affects the rate of replication fork progression.The Journal of cell biology · 2013Article
- G(1)/S and G(2)/M cyclin-dependent kinase activities commit cells to death in the absence of the S-phase checkpoint.Molecular and cellular biology · 2012Article
- Do replication forks control late origin firing in Saccharomyces cerevisiae?Nucleic acids research · 2012Article
- The DNA damage response pathway contributes to the stability of chromosome III derivatives lacking efficient replicators.PLoS genetics · 2010Article
- TORC1 kinase and the S-phase cyclin Clb5 collaborate to promote mitotic spindle assembly and DNA replication in S. cerevisiae.Current genetics · 2010Article
- How do Cdc7 and cyclin-dependent kinases trigger the initiation of chromosome replication in eukaryotic cells?Genes & development · 2010Review
- An overview of Cdk1-controlled targets and processes.Cell division · 2010Article
- Establishment of cohesion at the pericentromere by the Ctf19 kinetochore subcomplex and the replication fork-associated factor, Csm3.PLoS genetics · 2009Article
- Essential global role of CDC14 in DNA synthesis revealed by chromosome underreplication unrecognized by checkpoints in cdc14 mutants.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Cdc28/Cdk1 positively and negatively affects genome stability in S. cerevisiae.The Journal of cell biology · 2009Article
- The temporal program of chromosome replication: genomewide replication in clb5{Delta} Saccharomyces cerevisiae.Genetics · 2008Article
- Segmental duplications arise from Pol32-dependent repair of broken forks through two alternative replication-based mechanisms.PLoS genetics · 2008Article
- Rad53 regulates replication fork restart after DNA damage in Saccharomyces cerevisiae.Genes & development · 2008Article
- Identification of Clb2 residues required for Swe1 regulation of Clb2-Cdc28 in Saccharomyces cerevisiae.Genetics · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cyclin-dependent kinase (CDK) is required for the initiation of chromosomal DNA replication in eukaryotes. In Saccharomyces cerevisiae, the Clb5 and Clb6 cyclins activate Cdk1 and drive replication origin firing. Deletion of CLB5 reduces initiation of DNA synthesis from late-firing origins. We have examined whether checkpoints are activated by loss of Clb5 function and whether checkpoints are responsible for the DNA replication defects associated with loss of Clb5 function. We present evidence for activation of Rad53 and Ddc2 functions with characteristics suggesting the presence of DNA damage. Deficient late origin firing in clb5Delta cells is not due to checkpoint regulation, but instead, directly reflects the decreased abundance of S-phase CDK, as Clb6 activates late origins when its dosage is increased. Moreover, the viability of clb5Delta cells depends on Rad53. Activation of Rad53 by either Mrc1 or Rad9 contributes to the survival of clb5Delta cells, suggesting that both DNA replication and damage pathways are responsive to the decreased origin usage. These results suggest that reduced origin usage leads to stress or DNA damage at replication forks, necessitating the function of Rad53 in fork stabilization. Consistent with the notion that decreased S-CDK function creates stress at replication forks, deletion of RRM3 helicase, which facilitates replisome progression, greatly diminished the growth of clb5Delta cells. Together, our findings indicate that deregulation of S-CDK function has the potential to exacerbate genomic instability by reducing replication origin usage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.