During C. elegans embryogenesis, the DD, DA, and DB motor neurons arise from left and right lineages, move towards the midline and intercalate into a single tract to form the ventral nerve cord (VNC). Recently, the non-canonical Wnt-planar cell polarity was shown to regulate cell intercalation during VNC assembly. Disruption of this pathway causes DD neurons to shift anteriorly along the anterior-posterior (AP)-axis. Here, we investigated the role of the canonical Wnt-β-catenin pathway in positioning neurons in the VNC. Mutations in canonical Wnt pathway components, including bar-1/β-catenin and pop-1/TCF, cause the anterior displacement of DD2 towards DD1. In contrast, disruption of the β-catenin destruction complex gene pry-1/Axin results in the posterior displacement of DD1 towards DD2. In order to determine where and when defects occur, we used fluorescent time-lapse imaging to follow DD, DA and RIG neuroblasts during embryogenesis. In wild-type, we found that RIGL and DA2 intercalate between DD1 and DD2 via T1-type cell neighbor exchanges. Dorsal-ventral (DV) constriction of the DD1 and DD2 cell junction results in these cells meeting at a central vertex, which then resolves when the RIGL and DA2 cell junction expands along the AP axis. The resolution of the central vertex results in the spatial displacement of DD1 and DD2 along the AP axis. However, in Wnt-β-catenin mutants, central vertex resolution defects result in decreased spacing between DD1 and DD2 that persist into adulthood.