TOR controls transcriptional and translational programs via Sap-Sit4 protein phosphatase signaling effectors.

Published

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

  • 15367655

Electronic International Standard Serial Number (EISSN)

  • 1098-5549

International Standard Serial Number (ISSN)

  • 0270-7306

Digital Object Identifier (DOI)

  • 10.1128/MCB.24.19.8332-8341.2004

Language

  • eng