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Cell Death and Disease | Vol.10, Issue.12 | | Pages

Cell Death and Disease

Snail modulates JNK-mediated cell death in Drosophila

Chenxi Wu,Zhuojie Li,Xiang Ding,Xiaowei Guo,Ying Sun,Xingjun Wang,Yujia Hu,Tongtong Li,Xiaojin La,Jianing Li,Ji-an Li,Wenzhe Li,Lei Xue  
Abstract

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.

Original Text (This is the original text for your reference.)

Snail modulates JNK-mediated cell death in Drosophila

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.

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Chenxi Wu,Zhuojie Li,Xiang Ding,Xiaowei Guo,Ying Sun,Xingjun Wang,Yujia Hu,Tongtong Li,Xiaojin La,Jianing Li,Ji-an Li,Wenzhe Li,Lei Xue,.Snail modulates JNK-mediated cell death in Drosophila. 10 (12),.

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