Loading...
Thumbnail Image
Publication

Toll-9 interacts with Toll-1 to mediate a feedback loop during apoptosis-induced proliferation in Drosophila

Shields, Alicia
Amcheslavsky, Alla
Brown, Elizabeth
Lee, Tom V
Nie, Yingchao
Tanji, Takahiro
Ip, Y Tony
Bergmann, Andreas
Embargo Expiration Date
Abstract

Drosophila 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.

Source

Shields 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.

Year of Medical School at Time of Visit
Sponsors
Dates of Travel
DOI
10.1016/j.celrep.2022.110817
PubMed ID
35584678
Other Identifiers
Notes
Funding and Acknowledgements
Corresponding Author
Related Resources
Related Resources
Repository Citation
Rights
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/).Attribution-NonCommercial-NoDerivatives 4.0 International