期刊
CELL DIVISION
卷 15, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s13008-020-00062-5
关键词
Cell death; Drosophila; Toll; JNK; ROS
类别
资金
- National Natural Science Foundation of China [31771595, 31701244]
- Fundamental Research Funds for the Central Universities [20002150001, 22120180549]
- Natural Science Fund of Hebei Province of China [C2018209119]
- Scientific and Technological Research Project of Higher Education of Hebei Province [BJ2019040]
- Doctoral Scientific Research Foundation of North China University of Science and Technology [BS2017063]
Background Apoptosis plays pivotal roles in organ development and tissue homeostasis, with its major function to remove unhealthy cells that may compromise the fitness of the organism. Toll signaling, with the ancient evolutionary origin, regulates embryonic dorsal-ventral patterning, axon targeting and degeneration, and innate immunity. Using Drosophila as a genetic model, we characterized the role of Toll signaling in apoptotic cell death. Results We found that gain of Toll signaling is able to trigger caspase-dependent cell death in development. In addition, JNK activity is required for Toll-induced cell death. Furthermore, ectopic Toll expression induces the activation of JNK pathway. Moreover, physiological activation of Toll signaling is sufficient to produce JNK-dependent cell death. Finally, Toll signaling activates JNK-mediated cell death through promoting ROS production. Conclusions As Toll pathway has been evolutionarily conserved from Drosophila to human, this study may shed light on the mechanism of mammalian Toll-like receptors (TLRs) signaling in apoptotic cell death.
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