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

ABSTRACT: The Toll/NF-?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-?B pathway is essential for wound closure in late Drosophila embryos. Toll mutants and Dif dorsal (NF-?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-?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.

SUBMITTER: Carvalho L 

PROVIDER: S-EPMC4273363 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature