ORCID
- Claudia S. Barros: 0000-0003-0361-0333
- Torsten Bossing: 0000-0002-3277-9130
Abstract
Repair after traumatic injury often starts with mitotic activation around the lesion edges. Early midline cells in the Drosophila embryonic CNS can enter into division following the traumatic disruption of microtubules. We demonstrate that microtubule disruption activates non-canonical TNF signaling by phosphorylation of TGF-β activated kinase 1 (Tak1) and its target IkappaB kinase (Ik2), culminating in Dorsal/NfkappaB nuclear translocation and Jra/Jun expression. Tak1 and Ik2 are necessary for the damaged-induced divisions. Microtubule disruption caused by Tau accumulation is also reported in Alzheimer’s disease (AD). Human Tau expression in Drosophila midline cells is sufficient to induce Tak1 phosphorylation, Dorsal and Jra/Jun expression, and entry into mitosis. Interestingly, activation of Tak1 and Tank binding kinase 1 (Tbk1), the human Ik2 ortholog, and NfkappaB upregulation are observed in AD brains.
DOI Link
Publication Date
2021-07-06
Publication Title
Cell Reports
Volume
36
Issue
1
ISSN
2211-1247
Acceptance Date
2021-06-08
Deposit Date
2021-06-07
Embargo Period
2021-07-09
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
Recommended Citation
Barros, C., & Bossing, T. (2021) 'Microtubule disruption upon CNS damage triggers mitotic entry via TNF signaling activation', Cell Reports, 36(1). Available at: 10.1016/j.celrep.2021.109325
