Hobert and colleagues deduced this by studying the ventral nerve cord (VNC) in Caenorhabditis elegans. Development of the VNC is initiated by outgrowth of the PVT interneuron, which then secretes signals that direct growth of other VNC neurons. In the last decade, says Hobert, it was assumed that the important patterning factors were all made during embryonic development.
But in the new work, Hobert and colleagues have shown that ablation of the PVT in the first larval stage causes aberrant placement of axons across the ventral midline, even though growth of the axons was completed before ablation. Deletion of zig-4, which encodes an adhesion protein produced by the PVT, had similar effects. Fewer axons were affected than after ablation, however, suggesting that other zig family members may be important.
The maintenance mechanism may counteract stresses caused by mechanical forces. Loss of this maintenance mechanism could potentially be a factor in human neurodegenerative disease, as humans have proteins with a topology similar to that of the zig family proteins.