Abstract
The Drosophila cell-surface molecule connectin mediates cell-cell adhesion in vitro, and its expression pattern in vivo fits well with an adhesion role in the embryonic neuromuscular system. However, connectin mutants do not show dramatic neuromuscular defects, and ectopic expression studies so far have not supported an adhesion role. Here, we demonstrate that connectin mutants do have a phenotype; the normally connectin-positive pleural muscles fail to adhere closely together. An in vivo adhesion role is supported by misexpression studies, which result in excessive adhesion of normally connectin-negative muscles. Misexpression also causes defects in axon pathfinding. While a previous study interpreted similar defects as indicating a repulsion role for connectin, we argue that the phenotypes are consistent with connectin's adhesion role.
