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Basic Research Paper

A combined proteomic and genetic analysis identifies a role for the lipid desaturase Desat1 in starvation-induced autophagy in Drosophila

Katja Köhler Katja Köhler, Erich Brunner, Xue Li Guan, Karin Boucke, Urs F. Greber, Sonali Mohanty, Julia M.I. Barth, Markus R. Wenk and Ernst Hafen

Autophagy is a lysosomal-mediated degradation process that promotes cell survival during nutrient-limiting conditions. However, excessive autophagy results in cell death. In Drosophila, autophagy is regulated nutritionally, hormonally and developmentally in several tissues, including the fat body, a nutrient-storage organ. Here, we use a proteomics approach to identify components of starvation-induced autophagic responses in the Drosophila fat body. Using cICAT^TM labeling and mass spectrometry, differences in protein expression levels of normal compared to starved fat bodies were determined. Candidates were analyzed genetically for their involvement in autophagy in fat bodies deficient for the respective genes. One of these genes, Desat1, encodes a lipid desaturase. Desat1 mutant cells fail to induce autophagy upon starvation. The desat1 protein localizes to autophagic structures after nutrient depletion and is required for fly development. Lipid analyses revealed that Desat1 regulates the composition of lipids in Drosophila. We propose that Desat1 exerts its role in autophagy by controlling lipid biosynthesis and/or signaling necessary for autophagic responses.

Authors

Katja Köhler Katja Köhler

Institute of Molecular Systems Biology; Swiss Federal Institute of Technology Zürich; Zürich, Switzerland

Erich Brunner

Center for Model Organism Proteomes; University of Zürich; Zürich, Switzerland

Xue Li Guan

Department of Biochemistry and Department of Biological Sciences; Yong Loo Lin School of Medicine; National University of Singapore; Singapore

Karin Boucke

Institute of Zoology; University of Zürich; Zürich, Switzerland

Urs F. Greber

Institute of Zoology; University of Zürich; Zürich, Switzerland

Sonali Mohanty

Center for Model Organism Proteomes; University of Zürich; Zürich, Switzerland

Julia M.I. Barth

Institute of Molecular Systems Biology; Swiss Federal Institute of Technology Zürich; Zürich, Switzerland

Markus R. Wenk

Department of Biochemistry and Department of Biological Sciences; Yong Loo Lin School of Medicine; National University of Singapore; Singapore

Ernst Hafen Corresponding author: hafen@imsb.biol.ethz.ch

Institute of Molecular Systems Biology; Swiss Federal Institute of Technology Zürich; Zürich, Switzerland