Affordable Access

deepdyve-link
Publisher Website

Toll pathway is required for wound-induced expression of barrier repair genes in the Drosophila epidermis.

Authors
  • Capilla, Amalia1
  • Karachentsev, Dmitry1
  • Patterson, Rachel A1
  • Hermann, Anita1
  • Juarez, Michelle T2
  • McGinnis, William3
  • 1 Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093.
  • 2 Sophie Davis School Program of Biomedical Education, City University of New York School of Medicine, City College of New York, New York, NY 10031.
  • 3 Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093; [email protected]
Type
Published Article
Journal
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Publication Date
Mar 28, 2017
Volume
114
Issue
13
Identifiers
DOI: 10.1073/pnas.1613917114
PMID: 28289197
Source
Medline
Keywords
License
Unknown

Abstract

The epidermis serves as a protective barrier in animals. After epidermal injury, barrier repair requires activation of many wound response genes in epidermal cells surrounding wound sites. Two such genes in Drosophila encode the enzymes dopa decarboxylase (Ddc) and tyrosine hydroxylase (ple). In this paper we explore the involvement of the Toll/NF-κB pathway in the localized activation of wound repair genes around epidermal breaks. Robust activation of wound-induced transcription from ple and Ddc requires Toll pathway components ranging from the extracellular ligand Spätzle to the Dif transcription factor. Epistasis experiments indicate a requirement for Spätzle ligand downstream of hydrogen peroxide and protease function, both of which are known activators of wound-induced transcription. The localized activation of Toll a few cell diameters from wound edges is reminiscent of local activation of Toll in early embryonic ventral hypoderm, consistent with the hypothesis that the dorsal-ventral patterning function of Toll arose from the evolutionary cooption of a morphogen-responsive function in wound repair. Furthermore, the combinatorial activity of Toll and other signaling pathways in activating epidermal barrier repair genes can help explain why developmental activation of the Toll, ERK, or JNK pathways alone fail to activate wound repair loci.

Report this publication

Statistics

Seen <100 times