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

John R. Rohde, Susan Campbell, Sara A. Zurita-Martinez, N. Shane Cutler, Mark Ashe, Maria E. Cardenas

Research output: Contribution to journalArticlepeer-review

65 Citations (Scopus)

Abstract

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 2α 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.

Original languageEnglish
Pages (from-to)8332-8341
Number of pages10
JournalMolecular and Cellular Biology
Volume24
Issue number19
DOIs
Publication statusPublished - Oct 2004
Externally publishedYes

ASJC Scopus Subject Areas

  • Molecular Biology
  • Cell Biology

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

Fingerprint

Dive into the research topics of 'TOR controls transcriptional and translational programs via Sap-Sit4 protein phosphatase signaling effectors'. Together they form a unique fingerprint.

Cite this