ArticleMolecular biology of the cell1999
Protein kinase activity and identification of a toxic effector domain of the target of rapamycin TOR proteins in yeast.
Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Functional analysis of lncRNAs regulating the TOR signaling pathway and reproduction in the white-backed planthopper, Sogatella furcifera.Pest management science · 2026Article
- Article
- Article
- Article
- Phosphorylation of the TOR ATP binding domain by AGC kinase constitutes a novel mode of TOR inhibition.The Journal of cell biology · 2013Article
- Review
- Review series: TOR kinase complexes and cell migration.The Journal of cell biology · 2011Review
- Diverse environmental stresses elicit distinct responses at the level of pre-mRNA processing in yeast.RNA (New York, N.Y.) · 2011Article
- Target of rapamycin regulates development and ribosomal RNA expression through kinase domain in Arabidopsis.Plant physiology · 2011Article
- Conservation, duplication, and loss of the Tor signaling pathway in the fungal kingdom.BMC genomics · 2010Article
- Altered metabolism and persistent starvation behaviors caused by reduced AMPK function in Drosophila.PloS one · 2010Article
- Specific activation of mTORC1 by Rheb G-protein in vitro involves enhanced recruitment of its substrate protein.The Journal of biological chemistry · 2009Article
- Coordination of Ribosomal Protein and Ribosomal RNA Gene Expression in Response to TOR Signaling.Current genomics · 2009Article
- FGFR1 forms an FRS2-dependent complex with mTOR to regulate smooth muscle marker gene expression.Biochemical and biophysical research communications · 2009Article
- Contribution of natural inhibitors to the understanding of the PI3K/PDK1/PKB pathway in the insulin-mediated intracellular signaling cascade.International journal of molecular sciences · 2008Article
- Signaling cascades as drug targets in model and pathogenic fungi.Current opinion in investigational drugs (London, England : 2000) · 2008Review
- Golgi manganese transport is required for rapamycin signaling in Saccharomyces cerevisiae.Genetics · 2007Article
- Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.Genetics · 2007Article
- Synthesis and function of membrane phosphoinositides in budding yeast, Saccharomyces cerevisiae.Biochimica et biophysica acta · 2007Review
- Review
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Authors and funding
3 authors.
Funding
Abstract
In complex with FKBP12, the immunosuppressant rapamycin binds to and inhibits the yeast TOR1 and TOR2 proteins and the mammalian homologue mTOR/FRAP/RAFT1. The TOR proteins promote cell cycle progression in yeast and human cells by regulating translation and polarization of the actin cytoskeleton. A C-terminal domain of the TOR proteins shares identity with protein and lipid kinases, but only one substrate (PHAS-I), and no regulators of the TOR-signaling cascade have been identified. We report here that yeast TOR1 has an intrinsic protein kinase activity capable of phosphorylating PHAS-1, and this activity is abolished by an active site mutation and inhibited by FKBP12-rapamycin or wortmannin. We find that an intact TOR1 kinase domain is essential for TOR1 functions in yeast. Overexpression of a TOR1 kinase-inactive mutant, or of a central region of the TOR proteins distinct from the FRB and kinase domains, was toxic in yeast, and overexpression of wild-type TOR1 suppressed this toxic effect. Expression of the TOR-toxic domain leads to a G1 cell cycle arrest, consistent with an inhibition of TOR function in translation. Overexpression of the PLC1 gene, which encodes the yeast phospholipase C homologue, suppressed growth inhibition by the TOR-toxic domains. In conclusion, our findings identify a toxic effector domain of the TOR proteins that may interact with substrates or regulators of the TOR kinase cascade and that shares sequence identity with other PIK family members, including ATR, Rad3, Mei-41, and ATM.
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