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Autophagy. 2015;11(9):1471-83. doi: 10.1080/15548627.2015.1068488.

Expression of a ULK1/2 binding-deficient ATG13 variant can partially restore autophagic activity in ATG13-deficient cells.

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a Institute of Molecular Medicine I; Heinrich-Heine-University ; Düsseldorf , Germany.
b Department of Biochemistry and Molecular Biology ; Graduate School and Faculty of Medicine; University of Tokyo ; Tokyo , Japan.
c Department of Physiology and cell Biology ; Tokyo Medical and Dental University ; Tokyo , Japan.
d Center for Microbial Pathogenesis; The Research Institute at Nationwide Children's Hospital ; Columbus , OH USA.
e Department of Dermatology ; Medical Center; ZBSA Center for Biological Systems Analysis; BIOSS Centre for Biological Signaling Studies; Freiburg Institute for Advanced Studies; University of Freiburg ; Freiburg , Germany.
f Institute of Basic Medical Sciences; Faculty of Medicine; University of Oslo ; Oslo , Norway.


Autophagy describes an intracellular process responsible for the lysosome-dependent degradation of cytosolic components. The ULK1/2 complex comprising the kinase ULK1/2 and the accessory proteins ATG13, RB1CC1, and ATG101 has been identified as a central player in the autophagy network, and it represents the main entry point for autophagy-regulating kinases such as MTOR and AMPK. It is generally accepted that the ULK1 complex is constitutively assembled independent of nutrient supply. Here we report the characterization of the ATG13 region required for the binding of ULK1/2. This binding site is established by an extremely short peptide motif at the C terminus of ATG13. This motif is mandatory for the recruitment of ULK1 into the autophagy-initiating high-molecular mass complex. Expression of a ULK1/2 binding-deficient ATG13 variant in ATG13-deficient cells resulted in diminished but not completely abolished autophagic activity. Collectively, we propose that autophagy can be executed by mechanisms that are dependent or independent of the ULK1/2-ATG13 interaction.


ATG101; ATG13; RB1CC1; ULK1; autophagy

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