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Citation
Neufeld, T.P. (2007). Contribution of Atgl-dependent autophagy to TOR-mediated cell growth and survival.  Autophagy 3(5): 477--479.
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FBrf0201952
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Note
Abstract

The Ser/Thr kinase Atg1 (Ulk1/Unc51) appears to act as a convergence point for multiple signals that regulate autophagy, and in turn interacts with a large number of autophagy-related (Atg) proteins. Working in the Drosophila system, we recently found that overexpression of Atg1 is sufficient to induce autophagy, independent of upstream nutrient signals. We exploited this finding to examine the roles of autophagy in cell growth and death, and to test the interaction of Atg1 with the TOR signaling pathway. These studies provided genetic evidence that autophagy is a potent inhibitor of cell growth, and that high levels of autophagy lead to caspase-dependent apoptotic cell death in vivo. Atg1 also has an inhibitory effect on TOR signaling, indicating the existence of a positive feedback mechanism that may amplify the nutrient-dependent signals that control autophagy.

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Related Publication(s)
Research paper

Direct induction of autophagy by Atg1 inhibits cell growth and induces apoptotic cell death.
Scott et al., 2007, Curr. Biol. 17(1): 1--11 [FBrf0194462]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Autophagy
    Title
    Autophagy
    Publication Year
    2005-
    ISBN/ISSN
    1554-8627 1554-8635
    Data From Reference