Without this protein, motor axons do not properly enter their muscle target regions. This similarity suggests that Beat may normally work to oppose Fas II-mediated adhesivity and allow defasciculation of otherwise adherent sets of motor axons. The beat phenotype and its apparent antiadhesive function sheds light on the motoneuron outgrowth mechanism. At choice points, motor axons selectively defasciculate from the common pathway and steer into their muscle target region.
Several arguments suggest that defasciculation and steering are separable events.
The beat mutation affects all motoneuron defasciculation events, whereas mutations in genes involved in steering events might be expected to affect subsets of steering decisions. The strong genetic interactions between beat and genes coding for cell adhesion proteins, both expressed in motoneurons, are not consistent with a role in steering, which is presumably a motoneuron-target muscle interaction. Motoneurons would be expected to receive steering signals, not send them, and the secreted nature of Beat is not consistent with a receptor role. The common thread that runs through the phenotypes of the beat mutant and the misexpression experiments is that Beat interferes with cellular adhesive interactions. It seems more likely that Beat works through a receptor.