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


Köhler, K; Brunner, E; Guan, X L; Boucke, K; Greber, U F; Mohanty, S; Barth, J M; Wenk, M R; Hafen, E (2009). A combined proteomic and genetic analysis identifies a role for the lipid desaturase Desat1 in starvation-induced autophagy in Drosophila. Autophagy, 5(7):980-990.

Abstract

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() 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.

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() 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.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
Special Collections > SystemsX.ch
Special Collections > SystemsX.ch > Research, Technology and Development Projects > LipidX
Special Collections > SystemsX.ch > Research, Technology and Development Projects > WingX
08 University Research Priority Programs > Systems Biology / Functional Genomics
Dewey Decimal Classification:570 Life sciences; biology
Uncontrolled Keywords:autophagy, Drosophila, proteome, lipid
Language:English
Date:1 October 2009
Deposited On:19 Aug 2009 06:51
Last Modified:05 Apr 2016 13:19
Publisher:Landes Bioscience
ISSN:1554-8627
Additional Information:Verlags-PDF ist 12 Monaten nach Erscheinen beim Verlag offen zugänglich
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.4161/auto.5.7.9325
PubMed ID:19587536
Other Identification Number:NLM ID 10126518
Permanent URL: https://doi.org/10.5167/uzh-20191

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