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

• Autor(a) principal: Carvalho, Lara
• Data de Publicação: 2014
• Outros Autores: Jacinto, António, Matova, Nina
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10362/24296
• topic: Toll pathway; PROTEIN; NF-kappa B transcription factors; Drosophila; EMBRYO; IMMUNE-RESPONSE; ADHERENS JUNCTIONS; DORSAL-VENTRAL PATTERN; GRAINY-HEAD; epithelial wound repair; E-CADHERIN; GENE; POLARITY; E-cadherin; GRADIENT; Drosophila; E-cadherin; Epithelial wound repair; NF-κB transcription factors; Toll pathway

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.