Collective cell migration, which is movement of cells as a cohesive group, is a critical process during embryonic organ formation, wound healing and is inappropriately coopted during the invasion of certain cancers. Although many of the cellular hallmarks of collective cell migration have been defined, the genetic pathways that regulate these processes are not well understood. Development of the zebrafish lateral line has proven to be an elegant model for studying collective cell migration, as it is amenable to live imaging and genetic manipulation. The posterior lateral line (pLL) forms from the posterior lateral line primordium (pLLP), a cohort of ~100 cells which collectively migrate along the trunk of the developing zebrafish embryo. The pLLP is comprised of proliferative progenitor cells and organized epithelial cells that will form the hair cell-containing mechanosensory organs of the pLL. Wnt signaling is active in the leading progenitor zone of the pLLP and regulates cellular proliferation, survival and maintenance. Here we examine the downstream targets of Wnt signaling and their role in mediating pLLP progenitor cell behavior. We used RNA-sequencing to identify genes that are altered in zebrafish embryos carrying mutations in members of the canonical Wnt pathway that are known to regulate pLL formation, i.e. lef1 and kremen1, as compared to wild-type controls. One of the genes we selected for further analysis is the tumor suppressor Fat1b, which is strongly expressed in the wild-type pLLP and is downregulated following loss of Wnt signaling. CRISPR-Cas9-mediated mutation of Fat1b function results in failed pLLP migration in a manner that is similar to previously described canonical Wnt signaling mutants. These data suggest that our approach will allow us to refine our understanding of how canonical Wnt signaling pathway regulates various cellular behaviors.