Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance
Open accessAbstract
A Cre/ lox -conditional mouse line was generated to evaluate the role of ATR in checkpoint responses to ionizing radiation (IR) and stalled DNA replication. We demonstrate that after IR treatment, ATR and ATM each contribute to early delay in M-phase entry but that ATR regulates a majority of the late phase (2–9 h post-IR). Double deletion of ATR and ATM eliminates nearly all IR-induced delay, indicating that ATR and ATM cooperate in the IR-induced G2/M-phase checkpoint. In contrast to the IR-induced checkpoint, checkpoint delay in response to stalled DNA replication is intact in ATR knockout cells and ATR / ATM and ATR / p53 double-knockout cells. The DNA replication checkpoint remains intact in ATR knockout cells even though the checkpoint-stimulated inhibitory phosphorylation of Cdc2 on T14/Y15 and activating phosphorylation of the Chk1 kinase no longer occur. Thus, incomplete DNA replication in mammalian cells can prevent M-phase entry independently of ATR and inhibitory phosphorylation of Cdc2. When DNA replication inhibitors are removed, ATR knockout cells proceed to mitosis but do so with chromosome breaks, indicating that ATR provides a key genome maintenance function in S phase.
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ATR is an essential gene for nucleotide excision repair initiation and regulation and for genome maintenance.
“ATR is an essential gene for the initiation and regulation of NER and for genome maintenance 17, 36, 37.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [37]
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- Authors
- Brown, E. J., & Baltimore, D.
- Affiliations
- California Institute of Technology (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2003-02-19
- Volume
- 17
- Issue
- 5
- Pages
- 615-628
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC196009
- OpenAlex
- W2149687593
- Cited by
- 511
- References
- 46
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 6 · 2023: 14 · 2022: 10 · 2021: 19 · 2020: 19 · 2019: 15 · 2018: 18 · 2017: 19 · 2016: 17 · 2015: 21 · 2014: 26 · 2013: 26 · 2012: 19
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- National Cancer Institute (2R01CA51462-14, R01CA051462)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- ATR kinase, ATM kinase, G2/M checkpoint, DNA replication checkpoint, ionizing radiation response, cell cycle arrest, genome maintenance, Cdc2 phosphorylation, Chk1, chromosome breakage, p53, conditional knockout mice
- MeSH terms
- Checkpoint Kinase 1, Animals, Cell Cycle, DNA Damage, DNA-Binding Proteins, Mice, Transgenic, Protein Kinases, Radiation, Ionizing, Viral Proteins, CDC2 Protein Kinase, Protein Serine-Threonine Kinases, Mice, Knockout, Cell Cycle Proteins, Integrases, Tumor Suppressor Proteins, Mice, Ataxia Telangiectasia Mutated Proteins, Checkpoint Kinase 2
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