ArticleCell death & disease2019
Characterization of TNF-induced cell death in Drosophila reveals caspase- and JNK-dependent necrosis and its role in tumor suppression.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Epithelial cell competition is promoted by signaling from immune cells.Nature communications · 2025Article
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- Glial-derived TNF/Eiger signaling promotes somatosensory neurite sculpting.Cellular and molecular life sciences : CMLS · 2025Article
- Inhibition of pro-apoptotic UPR pathways PERK/CHOP and IRE1/JNK protects differentiated SH-SY5Y cells against rotenone-induced toxicity.Frontiers in molecular neuroscience · 2025Article
- Regeneration following tissue necrosis is mediated by non-apoptotic caspase activity.bioRxiv : the preprint server for biology · 2024Article
- Hippo effector, Yorkie, is a tumor suppressor in selectProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transient caspase-mediated activation of caspase-activated DNase causes DNA damage required for phagocytic macrophage differentiation.Cell reports · 2024Article
- Necrosensor: a genetically encoded fluorescent sensor for visualizing necrosis in Drosophila.Biology open · 2024Article
- Larval hematopoietic organs of multiplemicroPublication biology · 2024Article
- Cholinergic neurons trigger epithelial CaNature · 2023Article
- Understanding the diversity and dynamics of in vivo efferocytosis: Insights from the fly embryo.Immunological reviews · 2023Review
- Toll-9 interacts with Toll-1 to mediate a feedback loop during apoptosis-induced proliferation in Drosophila.Cell reports · 2022Article
- Non-apoptotic activation of Drosophila caspase-2/9 modulates JNK signaling, the tumor microenvironment, and growth of wound-like tumors.Cell reports · 2022Article
- Apoptosis Quantification in Tissue: Development of a Semi-Automatic Protocol and Assessment of Critical Steps of Image Processing.Biomolecules · 2021Article
- Drosophila as a model to explore secondary injury cascades after traumatic brain injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- The Duality of Caspases in Cancer, as Told through the Fly.International journal of molecular sciences · 2021Review
- Review
- The essential roles of Mps1 in spermatogenesis and fertility in mice.Cell death & disease · 2021Article
- Rab5 and Rab11 maintain hematopoietic homeostasis by restricting multiple signaling pathways ineLife · 2021Article
- Infection ofFrontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor-necrosis factor (TNF) and its superfamily members are pleiotropic cytokines. Activation of TNF can lead to distinct cellular outcomes including inflammation, cell survival, and different forms of cell death, such as apoptosis and necrosis in a context-dependent manner. However, our understanding of what determines the versatile functions of TNF is far from complete. Here, we examined the molecular mechanisms that distinguish the forms of cell death induced by Eiger (Egr), the sole homolog of TNF in Drosophila. We show that expression of Egr in the developing Drosophila eye simultaneously induces apoptosis and apoptosis-independent developmental defects indicated by cellular disorganization, both of which rely on the c-Jun N-terminal kinase (JNK) signaling activity. Intriguingly, when effector caspases DrICE and Dcp-1 are defective or inhibited, expression of Egr triggers necrosis which is characterized by loss of cell membrane integrity, translucent cytoplasm, and aggregation of cellular organelles. Moreover, such Egr-induced necrosis depends on the catalytic activity of the initiator caspase Dronc and the input from JNK signaling but is independent of their roles in apoptosis. Further mosaic analysis with mutants of scribble (scrib), an evolutionarily conserved tumor suppressor gene regulating cell polarity, suggests that Egr/JNK-mediated apoptosis and necrosis establish a two-layered defense system to inhibit the oncogenic growth of scrib mutant cells. Together, we have identified caspase- and JNK-dependent mechanisms underlying Egr-induced apoptosis versus necrosis and their fail-safe roles in tumor suppression in an intact organism in vivo.
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