ArticlePLoS biology2021
Dpp and Hedgehog promote the glial response to neuronal apoptosis in the developing Drosophila visual system.
Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- LncRNA modulates Dpp-mediated wing development to influence flight in Aedes aegypti.Cellular and molecular life sciences : CMLS · 2026Article
- Activated Hedgehog signaling in keratocytes leads to stromal stiffness and impairs corneal regeneration.NPJ Regenerative medicine · 2026Article
- Glial-derived TNF/Eiger signaling promotes somatosensory neurite sculpting.Cellular and molecular life sciences : CMLS · 2025Article
- Review
- Messenger functions of cell death during development and homeostasis.Biochemical Society transactions · 2023Article
- Glial regenerative response in the imaginal discs ofNeural regeneration research · 2023Article
- Review
- Dpp/TGFβ-superfamily play a dual conserved role in mediating the damage response in the retina.PloS one · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage in the nervous system induces a stereotypical response that is mediated by glial cells. Here, we use the eye disc of Drosophila melanogaster as a model to explore the mechanisms involved in promoting glial cell response after neuronal cell death induction. We demonstrate that these cells rapidly respond to neuronal apoptosis by increasing in number and undergoing morphological changes, which will ultimately grant them phagocytic abilities. We found that this glial response is controlled by the activity of Decapentaplegic (Dpp) and Hedgehog (Hh) signalling pathways. These pathways are activated after cell death induction, and their functions are necessary to induce glial cell proliferation and migration to the eye discs. The latter of these 2 processes depend on the function of the c-Jun N-terminal kinase (JNK) pathway, which is activated by Dpp signalling. We also present evidence that a similar mechanism controls glial response upon apoptosis induction in the leg discs, suggesting that our results uncover a mechanism that might be involved in controlling glial cells response to neuronal cell death in different regions of the peripheral nervous system (PNS).
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Registered trials
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