Abstract

Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via inactivation of the rapamycin-sensitive Tor complex1 (TORC1), a protein kinase complex regulating cell growth in response to nutrient conditions. However, the mechanism by which TORC1 controls autophagy and the direct target of TORC1 activity remain unclear. Atg13 is an essential regulatory component of autophagy upstream of the Atg1 kinase complex, and here we show that yeast TORC1 directly phosphorylates Atg13 at multiple Ser residues. Additionally, expression of an unphosphorylatable Atg13 mutant bypasses the TORC1 pathway to induce autophagy through activation of Atg1 in cells growing under nutrient-rich conditions. Our findings suggest that the direct control of the Atg1 complex by TORC1 induces autophagy.

Keywords

AutophagyAutophagy-related protein 13BiologyCell biologyBAG3TOR signalingKinaseProtein kinase ABiochemistryCyclin-dependent kinase 2Apoptosis

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Publication Info

Year
2009
Type
article
Volume
30
Issue
4
Pages
1049-1058
Citations
494
Access
Closed

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Yoshiaki Kamada, Kenichi Yoshino, Chika Kondo et al. (2009). Tor Directly Controls the Atg1 Kinase Complex To Regulate Autophagy. Molecular and Cellular Biology , 30 (4) , 1049-1058. https://doi.org/10.1128/mcb.01344-09

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DOI
10.1128/mcb.01344-09