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Citation
Glatter, T., Schittenhelm, R.B., Rinner, O., Roguska, K., Wepf, A., Jünger, M.A., Köhler, K., Jevtov, I., Choi, H., Schmidt, A., Nesvizhskii, A.I., Stocker, H., Hafen, E., Aebersold, R., Gstaiger, M. (2011). Modularity and hormone sensitivity of the Drosophila melanogaster insulin receptor/target of rapamycin interaction proteome.  Mol. Syst. Biol. 7(): 547.
FlyBase ID
FBrf0216604
Publication Type
Research paper
Abstract

Genetic analysis in Drosophila melanogaster has been widely used to identify a system of genes that control cell growth in response to insulin and nutrients. Many of these genes encode components of the insulin receptor/target of rapamycin (InR/TOR) pathway. However, the biochemical context of this regulatory system is still poorly characterized in Drosophila. Here, we present the first quantitative study that systematically characterizes the modularity and hormone sensitivity of the interaction proteome underlying growth control by the dInR/TOR pathway. Applying quantitative affinity purification and mass spectrometry, we identified 97 high confidence protein interactions among 58 network components. In all, 22% of the detected interactions were regulated by insulin affecting membrane proximal as well as intracellular signaling complexes. Systematic functional analysis linked a subset of network components to the control of dTORC1 and dTORC2 activity. Furthermore, our data suggest the presence of three distinct dTOR kinase complexes, including the evolutionary conserved dTTT complex (Drosophila TOR, TELO2, TTI1). Subsequent genetic studies in flies suggest a role for dTTT in controlling cell growth via a dTORC1- and dTORC2-dependent mechanism.

PubMed ID
PubMed Central ID
PMC3261712 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Mol. Syst. Biol.
    Title
    Molecular Systems Biology
    Publication Year
    2005-
    ISBN/ISSN
    1744-4292
    Data From Reference
    Alleles (7)
    Gene Groups (1)
    Genes (61)
    Physical Interactions (101)
    Datasets (4)
    Cell Lines (1)
    Transgenic Constructs (4)