ArticleCell death and differentiation2012
Role of the insulin/Tor signaling network in starvation-induced programmed cell death in Drosophila oogenesis.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
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- Integrated stress response signaling acts as a metabolic sensor in fat tissues to regulate oocyte maturation and ovulation.Cell reports · 2024Article
- Wdr59 promotes or inhibits TORC1 activity depending on cellular context.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Maternal starvation primes progeny response to nutritional stress.PLoS genetics · 2021Article
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- An RNAi screen of the kinome in epithelial follicle cells of the Drosophila melanogaster ovary reveals genes required for proper germline death and clearance.G3 (Bethesda, Md.) · 2021Article
- Effect of the interaction between ribosomal protein L10a and insulin receptor on carbohydrate metabolism.Heliyon · 2020Article
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- Spargel/dPGC-1 is essential for oogenesis and nutrient-mediated ovarian growth in Drosophila.Developmental biology · 2019Article
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- A visual screen for diet-regulated proteins in the Drosophila ovary using GFP protein trap lines.Gene expression patterns : GEP · 2017Article
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- Polarization of the epithelial layer and apical localization of integrins are required for engulfment of apoptotic cells in the Drosophila ovary.Disease models & mechanisms · 2015Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Amino-acid starvation leads to an inhibition of cellular proliferation and the induction of programmed cell death (PCD) in the Drosophila ovary. Disruption of insulin signaling has been shown to inhibit the progression of oogenesis, but it is unclear whether this phenotype mimics starvation. Here, we investigate whether the insulin-mediated phosphoinositide kinase-3 pathway regulates PCD in mid oogenesis. We reasoned that under well-fed conditions, disruption of positive components of the insulin signaling pathway within the germline would mimic starvation and produce degenerating egg chambers. Surprisingly, mutants did not mimic starvation but instead produced many abnormal egg chambers in which the somatic follicle cells disappeared and the germline persisted. These abnormal egg chambers did not show an induction of caspases and lysosomes like that observed in wild-type (WT) degenerating egg chambers. Egg chambers from insulin signaling mutants were resistant to starvation-induced PCD, indicating that a complete block in insulin-signaling prevents the proper response to starvation. However, target of rapamycin (Tor) mutants did show a phenotype that mimicked WT starvation-induced PCD, indicating an insulin independent regulation of PCD via Tor signaling. These results suggest that inhibition of the insulin signaling pathway is not sufficient to regulate starvation-induced PCD in mid oogenesis. Furthermore, starvation-induced PCD is regulated by Tor signaling converging with the canonical insulin signaling pathway.
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