TOR controls transcriptional and translational programs via Sap-Sit4 protein phosphatase signaling effectors.
Journal Article (Journal Article)
The Tor kinases are the targets of the immunosuppressive drug rapamycin and couple nutrient availability to cell growth. In the budding yeast Saccharomyces cerevisiae, the PP2A-related phosphatase Sit4 together with its regulatory subunit Tap42 mediates several Tor signaling events. Sit4 interacts with other potential regulatory proteins known as the Saps. Deletion of the SAP or SIT4 genes confers increased sensitivity to rapamycin and defects in expression of subsets of Tor-regulated genes. Sap155, Sap185, or Sap190 can restore these responses. Strains lacking Sap185 and Sap190 are hypersensitive to rapamycin, and this sensitivity is Gcn2 dependent and correlated with a defect in translation, constitutive eukaryotic initiation factor 2alpha hyperphosphorylation, induction of GCN4 translation, and hypersensitivity to amino acid starvation. We conclude that Tor signals via Sap-Sit4 complexes to control both transcriptional and translational programs that couple cell growth to amino acid availability.
Full Text
Duke Authors
Cited Authors
- Rohde, JR; Campbell, S; Zurita-Martinez, SA; Cutler, NS; Ashe, M; Cardenas, ME
Published Date
- October 2004
Published In
Volume / Issue
- 24 / 19
Start / End Page
- 8332 - 8341
PubMed ID
- 15367655
Pubmed Central ID
- PMC516738
International Standard Serial Number (ISSN)
- 0270-7306
Digital Object Identifier (DOI)
- 10.1128/MCB.24.19.8332-8341.2004
Language
- eng
Conference Location
- United States