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Updated: Jun 17, 2026
14:08
Study of Protein-protein Interactions in Autophagy Research
Published on: September 9, 2017
Tor directly controls the Atg1 kinase complex to regulate autophagy
Yoshiaki Kamada1, Ken-ichi Yoshino, Chika Kondo
1Division of Molecular Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan. yoshikam@nibb.ac.jp
Molecular and Cellular Biology
|December 10, 2009
Summary
Autophagy, essential for cell survival, is regulated by Tor complex1 (TORC1). This study reveals TORC1 directly phosphorylates Atg13, a key autophagy protein, controlling the process.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Autophagy is a crucial cellular degradation process vital for survival under starvation.
- Nutrient deprivation induces autophagy by inactivating the Tor complex1 (TORC1), a key regulator of cell growth.
- The precise mechanism of TORC1-mediated autophagy regulation and its direct targets are not fully understood.
Purpose of the Study:
- To elucidate the mechanism by which TORC1 controls autophagy.
- To identify the direct target of TORC1 activity in the autophagy pathway.
- To investigate the role of Atg13 phosphorylation in TORC1-mediated autophagy.
Main Methods:
- Investigated the interaction between TORC1 and Atg13 in yeast.
- Utilized site-directed mutagenesis to create an unphosphorylatable Atg13 mutant.
- Assessed autophagy induction and Atg1 activation under nutrient-rich conditions using the Atg13 mutant.
Main Results:
- Demonstrated that yeast TORC1 directly phosphorylates Atg13 at multiple serine residues.
- Showed that an Atg13 mutant, unable to be phosphorylated, bypasses TORC1 inhibition.
- Observed that this unphosphorylatable Atg13 mutant induces autophagy and activates Atg1 even in nutrient-rich conditions.
Conclusions:
- TORC1 directly regulates autophagy by phosphorylating Atg13, a component upstream of the Atg1 kinase complex.
- Phosphorylation of Atg13 by TORC1 is a critical step in suppressing autophagy under nutrient-rich conditions.
- Targeting Atg13 phosphorylation offers a potential mechanism for controlling autophagy induction.
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