DNA repair protein Rad55 is a terminal substrate of the DNA damage checkpoints
Open accessAbstract
Checkpoints, which are integral to the cellular response to DNA damage, coordinate transient cell cycle arrest and the induced expression of DNA repair genes after genotoxic stress. DNA repair ensures cellular survival and genomic stability, utilizing a multipathway network. Here we report evidence that the two systems, DNA damage checkpoint control and DNA repair, are directly connected by demonstrating that the Rad55 double-strand break repair protein of the recombinational repair pathway is a terminal substrate of DNA damage and replication block checkpoints. Rad55p was specifically phosphorylated in response to DNA damage induced by the alkylating agent methyl methanesulfonate, dependent on an active DNA damage checkpoint. Rad55p modification was also observed after gamma ray and UV radiation. The rapid time course of phosphorylation and the recombination defects identified in checkpoint-deficient cells are consistent with a role of the DNA damage checkpoint in activating recombinational repair. Rad55p phosphorylation possibly affects the balance between different competing DNA repair pathways.
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Checkpoints actively stimulate repair processes and, in higher eukaryotes, trigger apoptosis when damage cannot be successfully dealt with.
“The checkpoints also actively stimulate the repair processes [1–9] and, in higher eukaryotes, trigger the apoptotic response, if damage cannot be dealt with successfully [10–12].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [3]
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Self-citation
- Authors
- Bashkirov, V. I., King, J. S., Bashkirova, E. V., Schmuckli-Maurer, J., & Heyer, W.-D.
- Affiliations
- Russian Academy of Sciences (RU)
- Institute of General Microbiology
- University of California, Davis (US)
- Corresponding author
- Heyer, Wolf-Dietrich
- ORCID
- Heyer, Wolf-Dietrich
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2000-06-01
- Volume
- 20
- Issue
- 12
- Pages
- 4393-4404
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC85806
- OpenAlex
- W2121218667
- Cited by
- 164
- References
- 98
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 1 · 2021: 4 · 2019: 1 · 2018: 3 · 2017: 1 · 2016: 9 · 2015: 1 · 2014: 3 · 2013: 1 · 2012: 7
- FWCI
- 7.11
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Molecular and Cellular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- Rad55, DNA damage checkpoint, DNA repair, phosphorylation, recombinational repair, DNA double-strand break repair, methyl methanesulfonate, gamma radiation, ultraviolet radiation, recombination defects, cell cycle arrest, genome stability
- MeSH terms
- DNA Damage, DNA Repair, DNA-Binding Proteins, DNA, Fungal, Fungal Proteins, Phosphorylation, Recombination, Genetic, Saccharomyces cerevisiae, Ultraviolet Rays, Gene Expression Regulation, Fungal, Saccharomyces cerevisiae Proteins
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