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Article Addendum
Contribution of Atg1-Dependent Autophagy to TOR-Mediated Cell Growth and Survival
Thomas P. Neufeld
volume 3 | issue 5
September/October 2007Pages: 477 - 479
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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.
Addendum to:
Direct Induction of Autophagy by Atg1 Inhibits Cell Growth and Induces Apoptotic Cell Death
R.C. Scott, G. Juhász and T.P. Neufeld
Curr Biol 2007; 17:1-11
Authors
Thomas P. Neufeld
University of Minnesota
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.