ArticleMolecular and cellular biology2007
TOR signaling is a determinant of cell survival in response to DNA damage.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
55 citing papers in PubMed, 93 citations in OpenAlex.
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- Pharmacologic Induction of BRCAness inCancers · 2022Review
- A High-Copy Suppressor Screen Reveals a Broad Role of Prefoldin-like Bud27 in the TOR Signaling Pathway inGenes · 2022Article
- Deregulation of AKT-mTOR Signaling Contributes to Chemoradiation Resistance in Lung Squamous Cell Carcinoma.Molecular cancer research : MCR · 2022Article
- Genome-wide identification and expression analysis of sucrose nonfermenting-1-related protein kinase (SnRK) genes in Triticum aestivum in response to abiotic stress.Scientific reports · 2021Article
- Narrative review of emerging roles for AKT-mTOR signaling in cancer radioimmunotherapy.Annals of translational medicine · 2021Review
- LncRNA DINOR is a virulence factor and global regulator of stress responses in Candida auris.Nature microbiology · 2021Article
- Regulation of DNA duplication by the mTOR signaling pathway.Cell cycle (Georgetown, Tex.) · 2021Review
- Nuclear F-actin counteracts nuclear deformation and promotes fork repair during replication stress.Nature cell biology · 2020Article
- Inhibiting BRAF Oncogene-Mediated Radioresistance Effectively Radiosensitizes BRAFClinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Mck1 defines a key S-phase checkpoint effector in response to various degrees of replication threats.PLoS genetics · 2019Article
- The TOR Pathway Plays Pleiotropic Roles in Growth and Stress Responses of the Fungal PathogenGenetics · 2019Article
- Genome-wide identification and characterization of CKIN/SnRK gene family in Chlamydomonas reinhardtii.Scientific reports · 2019Article
- mTORC1/2 and Protein Translation Regulate Levels of CHK1 and the Sensitivity to CHK1 Inhibitors in Ewing Sarcoma Cells.Molecular cancer therapeutics · 2018Article
- The mTOR-S6K pathway links growth signalling to DNA damage response by targeting RNF168.Nature cell biology · 2018Article
- Ixr1 Regulates Ribosomal Gene Transcription and Yeast Response to Cisplatin.Scientific reports · 2018Article
- DNA damage regulates direct association of TOR kinase with the RNA polymerase II-transcribedMolecular biology of the cell · 2017Article
- P53 suppresses ribonucleotide reductase via inhibiting mTORC1.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The conserved TOR (target of rapamycin) kinase is part of a TORC1 complex that regulates cellular responses to environmental stress, such as amino acid starvation and hypoxia. Dysregulation of Akt-TOR signaling has also been linked to the genesis of cancer, and thus, this pathway presents potential targets for cancer chemotherapeutics. Here we report that rapamycin-sensitive TORC1 signaling is required for the S-phase progression and viability of yeast cells in response to genotoxic stress. In the presence of the DNA-damaging agent methyl methanesulfonate (MMS), TOR-dependent cell survival required a functional S-phase checkpoint. Rapamycin inhibition of TORC1 signaling suppressed the Rad53 checkpoint-mediated induction of ribonucleotide reductase subunits Rnr1 and Rnr3, thereby abrogating MMS-induced mutagenesis and enhancing cell lethality. Moreover, cells deleted for RNR3 were hypersensitive to rapamycin plus MMS, providing the first demonstration that Rnr3 contributes to the survival of cells exposed to DNA damage. Our findings support a model whereby TORC1 acts as a survival pathway in response to genotoxic stress by maintaining the deoxynucleoside triphosphate pools necessary for error-prone translesion DNA polymerases. Thus, TOR-dependent cell survival in response to DNA-damaging agents coincides with increased mutation rates, which may contribute to the acquisition of chemotherapeutic drug resistance.
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