The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
A reversible, p53-dependent G0/G1 cell cycle arrest induced by ribonucleotide depletion in the absence of detectable DNA damage.
Open accessAbstract
Cells with a functional p53 pathway undergo a G0/G1 arrest or apoptosis when treated with gamma radiation or many chemotherapeutic drugs. It has been proposed that DNA damage is the exclusive signal that triggers the arrest response. However, we found that certain ribonucleotide biosynthesis inhibitors caused a p53-dependent G0 or early G1 arrest in the absence of replicative DNA synthesis or detectable DNA damage in normal human fibroblasts. CTP, GTP, or UTP depletion alone was sufficient to induce arrest. In contrast to the p53-dependent response to DNA damage, characterized by long-term arrest and irregular cellular morphologies, the antimetabolite-induced arrest was highly reversible and cellular morphologies remained relatively normal. Both arrest responses correlated with prolonged induction of p53 and the Cdk inhibitor P21(WAF1/CIP1/SDI1) and with dephosphorylation of pRb. Thus, we propose that p53 can serve as a metabolite sensor activated by depletion of ribonucleotides or products or processes dependent on ribonucleotides. Accordingly, p53 may play a role in inducing a quiescence-like arrest state in response to nutrient challenge and a senescence-like arrest state in response to DNA damage. These results have important implications for the mechanisms by which p53 prevents the emergence of genetic variants and for developing more effective approaches to chemotherapy based on genotype.
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Cites
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Cited by
p53, the cellular gatekeeper for growth and division
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Metabolite profiling identifies a key role for glycine in rapid cancer cell proliferation
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Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells
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Awakening guardian angels: drugging the p53 pathway
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Metadata
- Authors
- Linke, S. P., Clarkin, K. C., Di Leonardo, A., Tsou, A., & Wahl, G. M.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1996-04-15
- Volume
- 10
- Issue
- 8
- Pages
- 934-947
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2021491682
- Cited by
- 538
- References
- 50
- Type
- posted content
- Language
- en
- Open access
- diamond
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- CoChat. (2026). Citation check: A reversible, p53-dependent G0/G1 cell cycle arrest induced by ribonucleotide depletion in the absence of detectable DNA damage. https://app.cochat.ai/papers/10.1101/gad.10.8.934
- The paper
- Linke, S. P., Clarkin, K. C., Di Leonardo, A., Tsou, A., & Wahl, G. M. (1996). A reversible, p53-dependent G0/G1 cell cycle arrest induced by ribonucleotide depletion in the absence of detectable DNA damage. Genes & Development. https://doi.org/10.1101/gad.10.8.934
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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