Toll signaling promotes JNK-dependent apoptosis in

Cell death Drosophila JNK ROS Toll

Journal

Cell division
ISSN: 1747-1028
Titre abrégé: Cell Div
Pays: England
ID NLM: 101251560

Informations de publication

Date de publication:
2020
Historique:
received: 01 11 2019
accepted: 29 02 2020
entrez: 17 3 2020
pubmed: 17 3 2020
medline: 17 3 2020
Statut: epublish

Résumé

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 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. As Toll pathway has been evolutionarily conserved from

Sections du résumé

BACKGROUND 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
RESULTS 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 CONCLUSIONS
As Toll pathway has been evolutionarily conserved from

Identifiants

pubmed: 32174999
doi: 10.1186/s13008-020-00062-5
pii: 62
pmc: PMC7063707
doi:

Types de publication

Journal Article

Langues

eng

Pagination

7

Informations de copyright

© The Author(s) 2020.

Déclaration de conflit d'intérêts

Competing interestsThe authors declare that they have no competing interests.

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Auteurs

Zhuojie Li (Z)

1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092 China.

Chenxi Wu (C)

1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092 China.
2College of Traditional Chinese Medicine, North China University of Science and Technology, 21 Bohai Road, Tangshan, 063210 China.

Xiang Ding (X)

1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092 China.

Wenzhe Li (W)

1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092 China.

Lei Xue (L)

1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092 China.
3Zhuhai Interventional Medical Center, Zhuhai Precision Medical Center, Zhuhai People's Hospital, Zhuhai Hospital Affiliated with Jinan University, Zhuhai, Guangdong 519000 China.

Classifications MeSH