page 757, Bosher et al. describe a set of critical reinforcements that allow C. elegans embryos to weather these forces rather than be torn apart. Besides illuminating a critical aspect of morphogenesis, the work establishes a new model for analyzing the coupling of tissues during development.
Using a genetic screen, the authors found that mutations in a locus called vab-10, which corresponds to spectraplakin, cause defects in the elongation of worm embryos. C. elegans vab-10 encodes two protein isoforms. Mutations that affect VAB-10A isoforms disrupt fibrous organelles, which are molecular and functional homologues of vertebrate hemidesmosomes. These mutations cause epidermal cells to detach from the cuticle and muscles during elongation. When VAB-10B isoforms are disrupted, the epidermis instead becomes thicker.
The results suggest that VAB-10A proteins allow epidermal cells to resist external stresses, whereas VAB-10B proteins ensure that the basal and apical membranes of the cells are locked a fixed distance apart, even in the presence of powerful internal stresses. The C. elegans system should now provide a useful platform to study how spectraplakins modulate and direct these forces. ▪