We are identifying molecules that function in the guidance of neuron growth cones along particular axonal pathways. Mutations in the
fax-1 (defective fasciculation of axons) gene cause disruptions in the pathfinding of growth cones along the ventral nerve cord (VNC). The AVKR, HSNL and PVQL growth cones normally extend along the left VNC bundle. In
fax-1 mutants these three growth cones are unable to recognize the left VNC bundle pathway, and extend inappropriately along the right VNC bundle. This defect is not a secondary consequence of faulty pioneering of the left VNC bundle, because the pioneer axon PVPR is present and appears normal. In order to understand the role of
fax-1 in directing growth cones, we cloned the gene. Genetic mapping localized
fax-1 to a region of the X chromosome between
unc-20 and
unc-78. Transformation rescue experiments demonstrated that
fax-1 resides on cosmid F56E3 and encodes a protein that bears a strong similarity to the retinoic acid receptor super-family of Zn-finger transcription factors. Therefore,
fax-1 may regulate the transcription of genes that mediate axon pathfinding. We are building GFP reporter fusions to determine in which neurons
fax-1 may function