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Autophagy in Drosophila ovaries is induced by starvation and is required for oogenesis
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Autophagy in Drosophila ovaries is induced by starvation and is required for oogenesis
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Journal Article
Autophagy in Drosophila ovaries is induced by starvation and is required for oogenesis
2011
Overview
Autophagy, an evolutionarily conserved lysosome-mediated degradation, promotes cell survival under starvation and is controlled by insulin/target of rapamycin (TOR) signaling. In
Drosophila
, nutrient depletion induces autophagy in the fat body. Interestingly, nutrient availability and insulin/TOR signaling also influence the size and structure of
Drosophila
ovaries, however, the role of nutrient signaling and autophagy during this process remains to be elucidated. Here, we show that starvation induces autophagy in germline cells (GCs) and in follicle cells (FCs) in
Drosophila
ovaries. This process is mediated by the ATG machinery and involves the upregulation of
Atg
genes. We further demonstrate that insulin/TOR signaling controls autophagy in FCs and GCs. The analysis of chimeric females reveals that autophagy in FCs, but not in GCs, is required for egg development. Strikingly, when animals lack
Atg
gene function in both cell types, ovaries develop normally, suggesting that the incompatibility between autophagy-competent GCs and autophagy-deficient FCs leads to defective egg development. As egg morphogenesis depends on a tightly linked signaling between FCs and GCs, we propose a model in which autophagy is required for the communication between these two cell types. Our data establish an important function for autophagy during oogenesis and contributes to the understanding of the role of autophagy in animal development.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Biology
/ Biomedical and Life Sciences
/ Cloning
/ Drosophila Proteins - genetics
/ Drosophila Proteins - metabolism
/ Female
/ Genes
/ Insects
/ Insulin
/ Kinases
/ Ovarian Follicle - metabolism
/ Ovaries
/ Signal Transduction - physiology
/ TOR Serine-Threonine Kinases - genetics
