期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 111, 期 50, 页码 E5373-E5382出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1408224111
关键词
Toll pathway; NF-kappa B transcription factors; epithelial wound repair; Drosophila; E-cadherin
资金
- Fundacao para a Ciencia e a Tecnologia, Portugal
- Marie Curie Fellowship [PIEF-GA-2009-255573]
- European Research Council [2007-StG-208631]
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.
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