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@ARTICLE{Udayakumar:308513,
      author       = {A. Udayakumar and F. Stavropoulos and T. Hadjipanteli and
                      G. Peng and S. Bahuguna$^*$ and C. MacClay and J. Y. Lee and
                      Q. Xiao and Y. Xia and M. Boutros$^*$ and J. Zhou and Y.
                      Apidianakis and C. Pitsouli and P. Ligoxygakis},
      title        = {{T}oll signalling controls intestinal regeneration in
                      {D}rosophila.},
      journal      = {Development},
      volume       = {153},
      number       = {2},
      issn         = {0022-0752},
      address      = {Cambridge},
      publisher    = {The Company of Biologists},
      reportid     = {DKFZ-2026-00153},
      pages        = {dev204794},
      year         = {2026},
      abstract     = {The intestinal interphase is where epithelial renewal and
                      tissue maintenance are balanced alongside immunological
                      regulation. How these functions integrate with cellular
                      signalling is under investigation. Here, we studied the role
                      of the evolutionarily conserved innate immune Toll/NF-κB
                      pathway in Drosophila intestinal regeneration. We found that
                      the core components of the canonical Toll pathway were
                      necessary for intestinal stem cell (ISC) mitosis in
                      homeostasis and upon infection. Toll activation was
                      sufficient to push ISCs into mitosis and the enteroblast
                      (EB) fate, but blocked EB differentiation resulting in ISC
                      and EB accumulation. This was mediated by JNK and Akt/TOR
                      signalling. When JNKK, JNK, Akt or TOR activity was reduced
                      in gut progenitors, ISC mitosis was suppressed. Toll
                      activation also triggered suppression of antimicrobial
                      lysozyme and amidase genes, which led to increased gut
                      bacterial density. Our results identify Toll as necessary
                      and sufficient for ISC mitosis. Our model is that the Toll
                      pathway acts as a regulator of the intestinal landscape
                      integrating JNK and Akt signals to achieve gut tissue
                      renewal and control of commensal bacteria density.},
      keywords     = {Animals / Drosophila Proteins: metabolism / Drosophila
                      Proteins: genetics / Toll-Like Receptors: metabolism /
                      Toll-Like Receptors: genetics / Intestines: physiology /
                      Intestines: cytology / Regeneration: physiology / Signal
                      Transduction / Mitosis / Stem Cells: cytology / Stem Cells:
                      metabolism / Drosophila melanogaster: physiology / Cell
                      Differentiation / Proto-Oncogene Proteins c-akt: metabolism
                      / NF-kappa B: metabolism / Drosophila (Other) / Gut (Other)
                      / Intestinal stem cells (Other) / Toll (Other) / Drosophila
                      Proteins (NLM Chemicals) / Toll-Like Receptors (NLM
                      Chemicals) / Tl protein, Drosophila (NLM Chemicals) /
                      Proto-Oncogene Proteins c-akt (NLM Chemicals) / NF-kappa B
                      (NLM Chemicals)},
      cin          = {B110},
      ddc          = {570},
      cid          = {I:(DE-He78)B110-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41552968},
      doi          = {10.1242/dev.204794},
      url          = {https://inrepo02.dkfz.de/record/308513},
}