ArticlePLoS biology2013
Two-tiered control of epithelial growth and autophagy by the insulin receptor and the ret-like receptor, stitcher.
Article in PLoS biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
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- Clemastine and hyperthermia enhance sensitization of osteosarcoma cells for apoptosis.Molecular & cellular oncology · 2024Article
- Review
- Functional requirements of protein kinases and phosphatases in the development of the Drosophila melanogaster wing.G3 (Bethesda, Md.) · 2021Article
- Autophagy suppresses Ras-driven epithelial tumourigenesis by limiting the accumulation of reactive oxygen species.Oncogene · 2017Article
- Exploring Autophagy in Drosophila.Cells · 2017Review
- Article
- Induction of Autophagy and Apoptosis via PI3K/AKT/TOR Pathways by Azadirachtin A in Spodoptera litura Cells.Scientific reports · 2016Article
- How and why to study autophagy in Drosophila: it's more than just a garbage chute.Methods (San Diego, Calif.) · 2015Article
- Neuronal control of metabolism through nutrient-dependent modulation of tracheal branching.Cell · 2014Article
- Autophagy in Drosophila: from historical studies to current knowledge.BioMed research international · 2014Review
- Toxoplasma gondii-induced activation of EGFR prevents autophagy protein-mediated killing of the parasite.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Body size in Drosophila larvae, like in other animals, is controlled by nutrition. Nutrient restriction leads to catabolic responses in the majority of tissues, but the Drosophila mitotic imaginal discs continue growing. The nature of these differential control mechanisms that spare distinct tissues from starvation are poorly understood. Here, we reveal that the Ret-like receptor tyrosine kinase (RTK), Stitcher (Stit), is required for cell growth and proliferation through the PI3K-I/TORC1 pathway in the Drosophila wing disc. Both Stit and insulin receptor (InR) signaling activate PI3K-I and drive cellular proliferation and tissue growth. However, whereas optimal growth requires signaling from both InR and Stit, catabolic changes manifested by autophagy only occur when both signaling pathways are compromised. The combined activities of Stit and InR in ectodermal epithelial tissues provide an RTK-mediated, two-tiered reaction threshold to varying nutritional conditions that promote epithelial organ growth even at low levels of InR signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.