Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Zurita-Martinez, SA; Puria, R; Pan, X; Boeke, JD; Cardenas, ME

Published Date

  • August 2007

Published In

Volume / Issue

  • 176 / 4

Start / End Page

  • 2139 - 2150

PubMed ID

  • 17565946

Pubmed Central ID

  • 17565946

International Standard Serial Number (ISSN)

  • 0016-6731

Digital Object Identifier (DOI)

  • 10.1534/genetics.107.072835

Language

  • eng

Conference Location

  • United States