Work

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

Year: 2017

Type: article

Abstract: 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.

Source: Proceedings of the National Academy of Sciences

DOI: 10.1073/pnas.1613917114

Authors: Amalia Capilla, Dmitry Karachentsev, Rachel A. Patterson, Anita Hermann, Michelle T. Juarez, William McGinnis

Institutions: University of California San Diego, City College of New York, City University of New York

Language: English

Topic: Invertebrate Immune Response Mechanisms

Subfield: Immunology

Field: Immunology and Microbiology

Domain: Life Sciences

Open Access status: green