Sema6A acts as a gate keeper at the VMEP by triggering the formation of BCC clusters. Our results support a model that suggests a role for Sema6A in BCC cluster initiation. (a) Motor axons leaving the ventral spinal cord express PlexinA1 on their surface (yellow rectangle). Boundary cap cells (blue circles) express Sema6A (green rectangles), which recognizes PlexinA1 on motor axons, resulting in the accumulation of BCCs and, subsequently, in their clustering. By an unknown mechanism the BCC cluster prevents motor neurons (red circles) but not motor axons from translocating into the periphery. (b, c) Consistent with this model, the absence of PlexinA1 from motor axons would remove the stop signal (b) and the absence of Sema6A from BCCs would remove the receptor for the stop signal (c). In both cases, BCC clusters would fail to form properly and motoneurons would not be confined to the ventral spinal cord but migrate into the periphery along the ventral roots. The behavior of sensory axons at the dorsal BCC clusters is more complex and cannot be fully explained by this model.