Snail modulates JNK-mediated cell death in Drosophila
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Updated: Jan 3, 2026
Morphological and Functional Evaluation of Axons and their Synapses during Axon Death in Drosophila melanogaster
Published on: March 16, 2020
Chenxi Wu1,2, Zhuojie Li1, Xiang Ding1
1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
Abstract:
Cell death plays a pivotal role in animal development and tissue homeostasis. Dysregulation of this process is associated with a wide variety of human diseases, including developmental and immunological disorders, neurodegenerative diseases and tumors. While the fundamental role of JNK pathway in cell death has been extensively studied, its down-stream regulators and the underlying mechanisms remain largely elusive. From a Drosophila genetic screen, we identified Snail (Sna), a Zinc-finger transcription factor, as a novel modulator of ectopic Egr-induced JNK-mediated cell death. In addition, sna is essential for the physiological function of JNK signaling in development. Our genetic epistasis data suggest that Sna acts downstream of JNK to promote cell death. Mechanistically, JNK signaling triggers dFoxO-dependent transcriptional activation of sna. Thus, our findings not only reveal a novel function and the underlying mechanism of Sna in modulating JNK-mediated cell death, but also provide a potential drug target and therapeutic strategies for JNK signaling-related diseases.
Insights
Researchers discovered Snail (Sna), a transcription factor, as a key regulator of JNK-mediated cell death in development. This finding offers new therapeutic targets for diseases linked to JNK signaling dysregulation.
Area of Science:
- Cellular Biology
- Developmental Biology
- Genetics
Background:
- Cell death is crucial for animal development and homeostasis, and its dysregulation is implicated in various human diseases.
- The JNK (c-Jun N-terminal kinase) pathway is vital for cell death, but its downstream effectors and mechanisms are not fully understood.
Purpose of the Study:
- To identify novel downstream regulators of JNK-mediated cell death.
- To elucidate the molecular mechanisms by which JNK signaling controls cell death during development.
Main Methods:
- Conducted a Drosophila genetic screen to identify new players in JNK-mediated cell death.
- Utilized genetic epistasis to determine the position of Snail (Sna) within the JNK signaling pathway.
- Investigated the transcriptional regulation of sna by JNK signaling and dFoxO.
Main Results:
- Identified Snail (Sna), a zinc-finger transcription factor, as a novel modulator of ectopic Egr-induced JNK-mediated cell death.
- Demonstrated that Sna is essential for the physiological role of JNK signaling in development.
- Showed that Sna acts downstream of JNK to promote cell death, with JNK signaling inducing dFoxO-dependent transcriptional activation of sna.
Conclusions:
- Revealed a novel function for Snail (Sna) in regulating JNK-mediated cell death.
- Elucidated a new mechanism where JNK signaling activates Sna transcriptionally via dFoxO.
- These findings suggest Sna and the JNK pathway as potential therapeutic targets for related human diseases.
