A lipid transfer protein ensures nematode cuticular impermeability
Ferdinand Ngale Njume, Adrià Razzauti, Miguel A. Soler, Veronika Perschin, Gholamreza Fazeli, Axelle Bourez, Cédric Delporte, Stephen Mbigha Ghogomu, Philippe Poelvoorde, Simon Pichard, Catherine Birck, Arnaud Poterszman, Jacob Souopgui, Pierre Van Antwerpen, Christian Stigloher, Luc Vanhamme, Patrick Laurent
Abstract
The cuticle of C. elegans is impermeable to chemicals, toxins and pathogens. However, increased permeability is a desirable phenotype because it facilitates chemical uptake. Surface lipids contribute to the permeability barrier. Here, we identify the lipid transfer protein GMAP-1 as a critical element setting the permeability of C. elegans cuticle. A gmap-1 deletion mutant increases cuticular permeability to sodium azide, levamisole, Hoechst and DiI. Expressing GMAP-1 in the hypodermis or transiently in the adults is sufficient to rescue this gmap-1 permeability phenotype. GMAP-1 protein is secreted from the hypodermis to the aqueous fluid filling the space between collagen fibres of the cuticle. In vitro, GMAP-1 protein binds Phosphatidyl-Serine and Phosphatidyl-Choline while in vivo, GMAP-1 sets the surface lipid composition and organisation. Altogether, our results suggest GMAP-1 secreted by hypodermis shuttles lipids to the surface to form the permeability barrier of C. elegans.