Growing axonal growth cones form actin-rich protrusions - filopodia - which extend the axon towards its target. Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) proteins are enriched at the tips of neuronal growth cone filopodia and are required for filopodia formation. Chemically induced elimination of filopodia in the developing vertebrate visual system causes misdirected axon growth. Cecile Lebrand and colleagues now show that, in the Xenopus developing visual system, reduced Ena/VASP protein activity in retinal ganglion cells (RGCs) does not affect axonal pathfinding, but does prevent the formation of branches in the optic tectum(). Lebrand and colleagues have eliminated Ena/VASP function in Xenopus RGCs by using a sequestration strategy that mislocalises these proteins to the mitochondrial membrane. Filopodia formation is drastically reduced in these retinal growth cones. Despite this, guidance errors do not occur, but growth cones advance slowly in the optic tract. Surprisingly, these proteins therefore seem to have a role in establishing terminal arborisations rather than in pathfinding; whether this is the case in other axonal pathways and organisms remains to be tested.
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