ArticleCell reports2022
Toll-9 interacts with Toll-1 to mediate a feedback loop during apoptosis-induced proliferation in Drosophila.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Toll receptors mediate tissue intrinsic surveillance against aberrant cells by detecting cell fate aberrations.Development (Cambridge, England) · 2026Article
- Calcium signaling regulates apoptosis-induced proliferation in Drosophila.PLoS biology · 2026Article
- The pxn-lgbp-ap-1 pathway restricts virus proliferation by inducing the expression of Cru1 in crayfish.Communications biology · 2025Article
- WNT signalling promotes NF-κB activation and drug resistance in KRAS-mutant colorectal cancer.EMBO reports · 2025Article
- Distinct roles of clustered MicroRNAs miR-286 and miR-6 in JNK activation critical to apoptosis-induced proliferation in Drosophila.Cellular and molecular life sciences : CMLS · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Hemocytes facilitate interclonal cooperation-induced tumor malignancy by hijacking the innate immune system in Drosophila.The EMBO journal · 2025Article
- Positional BMP signaling orchestrates villus length in the small intestine.Nature communications · 2025Article
- Article
- Activation of the Drosophila innate immune system accelerates growth in cooperation with oncogenic Ras.PLoS biology · 2025Article
- Functions ofFrontiers in cell and developmental biology · 2025Review
- Innate Immune Response ofInternational journal of molecular sciences · 2023Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
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.
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