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

ROHDE, John R, CAMPBELL, Susan, ZURITA-MARTINEZ, Sara A, CUTLER, N Shane, ASHE, Mark and CARDENAS, Maria E (2004). TOR controls transcriptional and translational programs via Sap-Sit4 protein phosphatase signaling effectors. Molecular and cellular biology, 24 (19), 8332-8341.

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Link to published version:: https://doi.org/10.1128/MCB.24.19.8332-8341.2004
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    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 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.

    Item Type: Article
    Research Institute, Centre or Group - Does NOT include content added after October 2018: Biomolecular Sciences Research Centre
    Identification Number: https://doi.org/10.1128/MCB.24.19.8332-8341.2004
    Page Range: 8332-8341
    Depositing User: Susan Campbell
    Date Deposited: 06 Aug 2014 08:24
    Last Modified: 06 Aug 2014 08:24
    URI: http://shura.shu.ac.uk/id/eprint/8299

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