Toll-9 interacts with Toll-1 to mediate a feedback loop during apoptosis-induced proliferation in Drosophila
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Lee, Tom V
Ip, Y Tony
UMass Chan AffiliationsMolecular, Cell and Cancer Biology
Program in Molecular Medicine
Document TypeJournal Article
KeywordsCP: Cell biology
nuclear translocation of dorsal
MetadataShow full item record
AbstractDrosophila Toll-1 and all mammalian Toll-like receptors regulate innate immunity. However, the functions of the remaining eight Toll-related proteins in Drosophila are not fully understood. Here, we show that Drosophila Toll-9 is necessary and sufficient for a special form of compensatory proliferation after apoptotic cell loss (undead apoptosis-induced proliferation [AiP]). Mechanistically, for AiP, Toll-9 interacts with Toll-1 to activate the intracellular Toll-1 pathway for nuclear translocation of the NF-κB-like transcription factor Dorsal, which induces expression of the pro-apoptotic genes reaper and hid. This activity contributes to the feedback amplification loop that operates in undead cells. Given that Toll-9 also functions in loser cells during cell competition, we define a general role of Toll-9 in cellular stress situations leading to the expression of pro-apoptotic genes that trigger apoptosis and apoptosis-induced processes such as AiP. This work identifies conceptual similarities between cell competition and AiP.
SourceShields A, Amcheslavsky A, Brown E, Lee TV, Nie Y, Tanji T, Ip YT, Bergmann A. Toll-9 interacts with Toll-1 to mediate a feedback loop during apoptosis-induced proliferation in Drosophila. Cell Rep. 2022 May 17;39(7):110817. doi: 10.1016/j.celrep.2022.110817. PMID: 35584678; PMCID: PMC9211775.
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/51750
RightsCopyright 2022 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).; Attribution-NonCommercial-NoDerivatives 4.0 International
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Except where otherwise noted, this item's license is described as Copyright 2022 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).