ArticleDevelopmental biology2014
A steroid-controlled global switch in sensitivity to apoptosis during Drosophila development.
Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- An atlas of caspase cleavage events in differentiating muscle cells.Protein science : a publication of the Protein Society · 2024Article
- Juvenile hormone-induced histone deacetylase 3 suppresses apoptosis to maintain larval midgut in the yellow fever mosquito.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Meep, a Novel Regulator of Insulin Signaling, Supports Development and Insulin Sensitivity via Maintenance of Protein Homeostasis inG3 (Bethesda, Md.) · 2020Article
- Polyploidy in the adulteLife · 2020Article
- Accurate elimination of superfluous attachment cells is critical for the construction of functional multicellular proprioceptors in Drosophila.Cell death and differentiation · 2019Article
- CDPs: caspase-dependent non-lethal cellular processes.Cell death and differentiation · 2017Article
- HDAC Inhibitors Disrupt Programmed Resistance to Apoptosis DuringG3 (Bethesda, Md.) · 2017Article
- Different cell cycle modifications repress apoptosis at different steps independent of developmental signaling in Drosophila.Molecular biology of the cell · 2016Article
- Nanos-mediated repression of hid protects larval sensory neurons after a global switch in sensitivity to apoptotic signals.Development (Cambridge, England) · 2016Article
- miR-8 modulates cytoskeletal regulators to influence cell survival and epithelial organization in Drosophila wings.Developmental biology · 2016Article
- Ligand-independent requirements of steroid receptors EcR and USP for cell survival.Cell death and differentiation · 2016Article
- Xrn1/Pacman affects apoptosis and regulates expression of hid and reaper.Biology open · 2015Article
- Cell death in development: Signaling pathways and core mechanisms.Seminars in cell & developmental biology · 2015Review
- Regulation of Cell Death by IAPs and Their Antagonists.Current topics in developmental biology · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Precise control over activation of the apoptotic machinery is critical for development, tissue homeostasis and disease. In Drosophila, the decision to trigger apoptosis--whether in response to developmental cues or to DNA damage--converges on transcription of inhibitor of apoptosis protein (IAP) antagonists reaper, hid and grim. Here we describe a parallel process that regulates the sensitivity to, rather than the execution of, apoptosis. This process establishes developmental windows that are permissive or restrictive for triggering apoptosis, where the status of cells determines their capacity to die. We characterize one switch in the sensitivity to apoptotic triggers, from restrictive to permissive, that occurs during third-instar larval (L3) development. Early L3 animals are highly resistant to induction of apoptosis by expression of IAP-antagonists, DNA-damaging agents and even knockdown of the IAP diap1. This resistance to apoptosis, however, is lost in wandering L3 animals after acquiring a heightened sensitivity to apoptotic triggers. This switch in sensitivity to death activators is mediated by a change in mechanisms available for activating endogenous caspases, from an apoptosome-independent to an apoptosome-dependent pathway. This switch in apoptotic pathways is regulated in a cell-autonomous manner by the steroid hormone ecdysone, through changes in expression of critical pro-, but not anti-, apoptotic genes. This steroid-controlled switch defines a novel, physiologically-regulated, mechanism for controlling sensitivity to apoptosis and provides new insights into the control of apoptosis during development.
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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.