Together with zig-5, required postembryonically to maintain the position of ASI and ASH head neuron cell bodies and ventral nerve cord axons of PVQ, PVP and HSN neurons by preventing their displacement that could occur during body growth and movement. May act by reducing L1CAM-like protein sax-7 (long isoform) adhesion. Expressed in PVT neurons and pharyngeal muscles. Expression begins at the late L1 larval stage. No visible phenotype. In a zig-5 mutant background, 74 percent of animals have cell bodies of ASI and ASH head neurons displaced either on the top of or anterior to the nerve ring. In addition, double mutants show defects in the positioning of the ventral nerve cord (VNC) axons characterized by axons of embryonically generated PVQ, PVP and HSN neurons from the left and right VNC drifting into the opposite cord (axon flip-over). Both defects begin at the L3 larval stage and become more pronounced at the L4 larval and adult stages. Cell body and axon positioning is normal in embryos and in L1 larvae. In a zig-1, zig-2, zig-3 or zig-4 mutant background, cell body positioning of ASI and ASH head neurons is normal. In unc-13 or unc-54 mutant background, where locomotion is impaired, cell body positioning of ASI and ASH neurons is normal. In a sax-7 (nj53) mutant background, cell body and axon positioning is normal. Simultaneous RNAi-mediated knockdown of zig-5 and zig-8 at the embryonic, larval or adult stage causes a displacement of ASI and ASH head neurons in 6 to 9 percent of animals.