Hypothetical model of Fignl1-mediated regulation of dynein-based retrograde transport velocity during motor axon pathfinding. (A and B) Left-hand panels schematize the physiological consequences of Fignl1 loss of function (B) on SMN axon pathfinding compared with normal conditions (A). Schemes represent lateral views of two zebrafish hemisegments, anterior to the left. Ant, anterior; Post, posterior. Boxed right-hand panels focus on the molecular model that might underlie SMN navigational behavior in each condition. (A) In healthy conditions, Fignl1 may promote the recruitment of Kif1bβ onto dynein-bound cargoes—or vice versa—which could decrease the velocity of the dynein/dynactin complex through a tug of war or a cooperative mechanism. Fignl1-mediated inhibition of dynein velocity may then regulate the delivery of cargoes required for accurate rostral nerve targeting. (B) Fignl1 depletion could reduce the number of dynein-attached cargoes associated with Kif1bβ and would thus increase dynein-mediated retrograde axonal transport velocity, ultimately affecting the distribution of cargoes critical for rostral nerve fasciculation and pathfinding.