Neuronal migration is a key mechanism during neural development, as it allows cells to reach their final destination, establishing the basis for the subsequent wiring of neural circuitry. Collective cell migration, the coordinated migration of a cell population through cell–cell contact, is a recognized mode of migration for a variety of cell types, but its role in neuronal migration has been poorly characterized. We have recently published that facial branchiomotor (FBM) neurons, that migrate from rhombomere (r)4 to r6 in the developing hindbrain, use a collective mode of migration in which one FBM neuron can influence the migration of neighboring FBM neurons presumably through cell-cell contact. Here, we examined whether N-cadherin is a candidate cell adhesion molecule mediating the collective migration of FBM neurons. To accomplish this, we generated stable transgenic fish expressing a dominant-negative N-cadherin, lacking the extracellular domain (ncadhDEC), specifically in cranial branchiomotor neurons using the islet1 promoter. We find that caudal migration of FBM neurons is blocked in Tg(isl1: ncadhDEC) fish, as they fail to exit r4. Timelapse imaging revealed that loss of N-cadherin function does not block cell motility as FBM neurons migrate randomly and dorsally within r4. To determine whether N-cadherin is required for collective migration, we generated mosaic embryos in which some FBM neurons expressed ncadhDEC adjacent to wild-type FBM neurons. We found that few, if any, ncadhDEC-expressing FBM neurons could be rescued via collective migration by neighboring wild-type neurons. Taken together, our data suggest that N-cadherin plays an essential cell-autonomous role in mediating the collective migration of FBM neurons.