Perspectives on the DNA damage and replication checkpoint responses in Saccharomyces cerevisiae
Open accessAbstract
The DNA damage and replication checkpoints are believed to primarily slow the progression of the cell cycle to allow DNA repair to occur. Here we summarize known aspects of the Saccharomyces cerevisiae checkpoints including how these responses are integrated into downstream effects on the cell cycle, chromatin, DNA repair, and cytoplasmic targets. Analysis of the transcriptional response demonstrates that it is far more complex and less relevant to the repair of DNA damage than the bacterial SOS response. We also address more speculative questions regarding potential roles of the checkpoint during the normal S-phase and how current evidence hints at a checkpoint activation mechanism mediated by positive feedback that amplifies initial damage signals above a minimum threshold.
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The DNA damage checkpoint response is a signal transduction cascade based mainly on phosphorylation events.
“The DNA damage checkpoint response consists of a signal transduction cascade mainly based on phosphorylation events; the mechanistic details of the pathway have been recently discussed elsewhere [15,16]”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [15]
In budding yeast, Mec1 is the main checkpoint activator after all DNA lesions, while Tel1 is mainly devoted to telomere maintenance; Tel1's redundant checkpoint role appears only without Mec1.
“This separation of tasks is not found in budding yeast, where Mec1 (the ATR homologue) is the main player of checkpoint activation after all kind of DNA lesions, while Tel1 (the ATM homologue) is especially devoted to telomere maintenance. The redundant role of Tel1 in the DNA damage checkpoint is uncovered only in the absence of Mec1 [15,43].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [15]
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References 137 · Cited by 83
- Authors
- Putnam, C. D., Jaehnig, E. J., & Kolodner, R. D.
- Affiliations
- Ludwig Cancer Research (BE)
- University of California San Diego (US)
- Corresponding author
- Putnam, Christopher D.
- Venue
- DNA Repair
- Publisher
- Elsevier BV
- Published
- 2009-09-02
- Volume
- 8
- Issue
- 9
- Pages
- 974-982
- ISSN
- 1568-7856 (ISSN-L)
- 1568-7864
- PMC
- PMC2725198
- OpenAlex
- W1993755338
- Cited by
- 83
- References
- 137
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 6 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 10 · 2012: 12
- FWCI
- 4.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- DNA repair (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (GM-26017, R37GM026017, R01GM026017)
- National Institute of Environmental Health Sciences (ES014811, R01ES014811)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Keywords
- DNA damage checkpoint, S-phase checkpoint, Saccharomyces cerevisiae, cell cycle arrest, chromatin, transcriptional response, SOS response, S phase, positive feedback, checkpoint activation, signal amplification
- MeSH terms
- Cell Cycle, DNA Damage, DNA Replication, Saccharomyces cerevisiae, Feedback, Physiological
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