The Toll/NF-kappa B signaling pathway is required for epidermal wound repair in Drosophila

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The Toll/NF-kappa B pathway, first identified in studies of dorsal-ventral polarity in the early Drosophila embryo, is well known for its role in the innate immune response. Here, we reveal that the Toll/NF-kappa B pathway is essential for wound closure in late Drosophila embryos. Toll mutants and Dif dorsal (NF-kappa B) double mutants are unable to repair epidermal gaps. Dorsal is activated on wounding, and Dif and Dorsal are required for the sustained down-regulation of E-cadherin, an obligatory component of the adherens junctions (AJs), at the wound edge. This remodeling of the AJs promotes the assembly of an actin-myosin cable at the wound margin; contraction of the actin cable, in turn, closes the wound. In the absence of Toll or Dif and dorsal (dl), both E-cadherin down-regulation and actin-cable formation fail, thus resulting in open epidermal gaps. Given the conservation of the Toll/NF-kappa B pathway in mammals and the epithelial expression of many components of the pathway, this function in wound healing is likely to be conserved in vertebrates.
Original languageEnglish
Pages (from-to)5373-5382
Number of pages10
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number50
Publication statusPublished - 16 Dec 2014


  • Drosophila
  • E-cadherin
  • Epithelial wound repair
  • NF-κB transcription factors
  • Toll pathway


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