ArticleApoptosis : an international journal on programmed cell death2019
Ultraspiracle-independent anti-apoptotic function of ecdysone receptors is required for the survival of larval peptidergic neurons via suppression of grim expression in Drosophila melanogaster.
Article in Apoptosis : an international journal on programmed cell death, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Astrocyte-dependent local neurite pruning in Beat-Va neurons.The Journal of cell biology · 2025Article
- Regional specialization, polyploidy, and seminal fluid transcripts in theProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Drosophila postembryonic nervous system development: a model for the endocrine control of development.Genetics · 2023Review
- Reproductive Outbreaks ofInternational journal of molecular sciences · 2022Article
- Review
- Programmed cell death reshapes the central nervous system during metamorphosis in insects.Current opinion in insect science · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
In Drosophila melanogaster a significant number of heterogenous larval neurons in the central nervous system undergo metamorphosis-associated programmed cell death, termed metamorphoptosis. Interestingly distinct groups of doomed larval neurons are eliminated at different metamorphic phases. Although ecdysone hormonal signaling via nuclear ecdysone receptors (EcRs) is known to orchestrate the neuronal metamorphoptosis, little is known about how this signaling controls such diverse neuronal responses. Crustacean cardioactive peptide (CCAP)-producing neurons in the ventral nerve cord are developmentally programmed to die shortly after adult emergence. In this study, we show that disruption of endogenous EcR function by ectopic expression of dominant negative forms of EcRs (EcR
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