An Imperfect G 2 M Checkpoint Contributes to Chromosome Instability Following Irradiation of S and G 2 Phase Cells
Open accessAbstract
DNA double strand break (DSB) repair and checkpoint control represent two major mechanisms that function to reduce chromosomal instability following ionizing irradiation (IR). Ataxia telangiectasia (A-T) cells have long been known to have defective checkpoint responses. Recent studies have shown that they also have a DSB repair defect following IR raising the issue of how ATM's repair and checkpoint functions interplay to maintain chromosomal stability. A-T and Artemis cells manifest an identical and epistatic repair defect throughout the cell cycle demonstrating that ATM's major repair defect following IR represents Artemis-dependent end-processing. Artemis cells show efficient G(2)/M checkpoint induction and a prolonged arrest relative to normal cells. Following irradiation of G(2) cells, this checkpoint is dependent on ATM and A-T cells fail to show checkpoint arrest. In contrast, cells irradiated during S phase initiate a G(2)/M checkpoint which is independent of ATM and, significantly, both Artemis and A-T cells show a prolonged arrest at the G(2)/M checkpoint likely reflecting their repair defect. Strikingly, the G(2)/M checkpoint is released before the completion of repair when approximately 10-20 DSBs remain both for S phase and G(2) phase irradiated cells. This defined sensitivity level of the G(2)/M checkpoint explains the prolonged arrest in repair-deficient relative to normal cells and provides a conceptual framework for the cooperative phenotype between checkpoint and repair functions in maintaining chromosomal stability.
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Cells with a low number of DNA breaks can enter mitosis.
“Therefore, cells with a low number of DNA breaks can enter mitosis [103,104].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [104]
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- Authors
- Krempler, A., Deckbar, D., Jeggo, P. A., & Lobrich, M.
- Affiliations
- Saarland University (DE)
- University of Sussex (GB)
- ORCID
- Jeggo, Penny A.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2007-07-15
- Volume
- 6
- Issue
- 14
- Pages
- 1682-1686
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2054949155
- Cited by
- 109
- References
- 32
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 4 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 4 · 2014: 8 · 2013: 8 · 2012: 10
- FWCI
- 0.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Sussex Research Online (University of Sussex) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Wilhelm Sander-Stiftung
- Deutsche Forschungsgemeinschaft (LO 677/4-1/2)
- Bundesministerium für Bildung und Forschung (02S8335, 02S8355)
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- G2/M checkpoint, chromosomal instability, ionizing radiation, DNA double-strand break repair, ATM, ataxia telangiectasia, Artemis, S-phase checkpoint, DNA end processing
- MeSH terms
- Cell Division, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Endonucleases, Humans, Nuclear Proteins, Radiation, Ionizing, G2 Phase, S Phase, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Tumor Suppressor Proteins, Chromosomal Instability, Ataxia Telangiectasia Mutated Proteins
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