Semaphorin-1a Acts in Concert With the Cell Adhesion Molecules Fasciclin II and Connectin to Regulate Axon Fasciculation in Drosophila

Corresponding author: Alex L. Kolodkin, Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 N. Wolfe St./813 WBSB, Baltimore, MD 21205., kolodkin{at}jhmi.edu (E-mail)

Communicating editor: K. ANDERSON

Semaphorins comprise a large family of phylogenetically conserved secreted and transmembrane glycoproteins, many of which have been implicated in repulsive axon guidance events. The transmembrane semaphorin Sema-1a in Drosophila is expressed on motor axons and is required for the generation of neuromuscular connectivity. Sema-1a can function as an axonal repellent and mediates motor axon defasciculation. Here, by manipulating the levels of Sema-1a and the cell adhesion molecules fasciclin II (Fas II) and connectin (Conn) on motor axons, we provide further evidence that Sema-1a mediates axonal defasciculation events by acting as an axonally localized repellent and that correct motor axon guidance results from a balance between attractive and repulsive guidance cues expressed on motor neurons.

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