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| Jun (2007); 0: | |
| Efficient Tor signaling requires a functional Class C Vps protein complex in saccharomyces cerevisiae- | |
| Zurita-Martinez SA, Puria R, Pan X, Boeke JD, Cardenas ME | |
| Duke University Medical Center- | |
| Abstract: The Tor kinases regulate responses to nutrients and control cell growth- Unlike most organisms that only contain one Tor protein, Saccharomyces cerevisiae expresses two, Tor1 and Tor2, which are thought to share all of the rapamycin-sensitive functions attributable to Tor signaling- Here we conducted a genetic screen that defined the global TOR1 synthetic fitness or lethal interaction gene network- This screen identified mutations in distinctive functional categories that impaired vacuolar function, including components of the EGO-Gse and PAS complexes that reduce fitness- In addition, tor1 is lethal in combination with mutations in class C Vps complex components- We find that Tor1 does not regulate the known function of the class C Vps complex in protein sorting- Instead class C vps mutants fail to recover from rapamycin-induced growth arrest or to survive nitrogen starvation and have low levels of amino acids- Remarkably, addition of glutamate or glutamine restores viability to a tor1 pep3 mutant strain- We conclude that Tor1 is more effective than Tor2 at providing rapamycin-sensitive Tor signaling under conditions of amino acid limitation, and that an intact class C Vps complex is required to mediate intracellular amino acid homeostasis for efficient Tor signaling- | |
| [PUBMED: 17565946] |   |
| Copyright © 2009, Tyers Lab, The Samuel Lunenfeld Research Institute, Mount Sinai Hospital, All Rights Reserved. |
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| BioGRID: A General Repository for Interaction Datasets. Chris Stark, Bobby-Joe Breitkreutz, Teresa Reguly, Lorrie Boucher, Ashton Breitkreutz, Mike Tyers. Nucleic Acids Res. Jan 1;34:D535-9. |