Neural crest cells (NCCs) are a impressive, dynamic group of cells that travel long distances in the embryo to reach their target sites. GTPase, ephrin, PCP signaling, cadherin, VEGF Neural crest cells (NCCs) are a pluripotent human population of cells that migrate from the dorsal neuroepithelium and give rise to multiple cell types including neurons and glia of the peripheral nervous system, pigment cells and craniofacial bone tissue and cartilage.1 An important characteristic of NCCs is their impressive ability to migrate over long distances HA14-1 and along specific pathways through the embryo. NCC migration begins with an epithelial to mesenchymal transition (EMT), in which NCCs shed adhesions with their neighbors and segregate from the neuroepithelium.2,3 Following EMT, NCCs acquire a polarized morphology and initiate directed migration away from the neural tube. While migrating along their pathways to their target cells, NCCs are led by considerable communication with one another and by additional cues from the extracellular environment. Each of these elements of NCC migration requires exact legislation of cell motile behaviors, although the mechanisms controlling them are still not well recognized. A essential step toward understanding the molecular HA14-1 control of NCC motility is definitely characterization of NCC behaviors as they migrate in their native environment. In the recent 15 years, multiple studies possess analyzed specific behaviours connected with NCCs along the numerous phases of their journey and have begun to determine substances controlling these behaviours. In this review we will focus specifically on these studies that use live imaging and will focus on the strength of live imaging to reveal mechanisms regulating NCC motility and migration pathways. Epithelial to Mesenchymal Transition The onset of aimed NCC migration is definitely preceded by EMT, which is definitely a dramatic, multistep process wherein cells shed epithelial adhesions, acquire motility and segregate from the neuroepithelium.2,3 Only some cells in the neuroepithelium become NCCs and undergo EMT, while others remain in the neuroepithelium and become part of the HA14-1 central nervous system. Therefore, NCCs must disassemble adhesions while additional neighboring cells maintain them. Precise legislation of these dynamic processes is definitely consequently essential for appropriate development of both the neural tube and NCC derivatives, yet how they are matched and controlled in vivo remains poorly recognized. Two recent studies possess used live imaging to characterize NCC behaviors before and during EMT while cells are in their native environment. These studies of either zebrafish cranial NCCs in vivo4 or of chick trunk NCCs in a semi-intact slice preparation5 possess defined specific cell behaviors underlying EMT and have offered book insight into mechanisms of EMT. Ahlstrom and Erickson5 used long-term imaging in slices to examine the behavior of chick trunk NCCs within the neuroepithelium before EMT. Neuroepithelial cells and premigratory NCCs span the width of the pseudo-stratified neuroepithelium HA14-1 with adherens junction attachments at the apical surface (Fig. 1A). There have been several proposed hypotheses of how NCCs break their cell attachments within the neuroepithelium to allow EMT to happen. One hypothesis is definitely that apical adhesions must become downregulated or disassembled and that this loss of adhesion is definitely the traveling push in NCC EMT.6C9 On the other hand, NCCs may be able to generate enough motile force to break away from HA14-1 adhesions without the need to downregulate them.10,11 Ahlstrom and Erickson5 found that premigratory NCCs usually shed their apical attachments and parts of adherens junctions before retraction of the apical tail and translocation out of the neural tube (Fig. 1A and cell 1a). This is definitely not constantly the case however, as occasionally junctional FJX1 parts were still present after detachment and migrated along with the retracting tail (Fig. 1A and cell 1b). Hardly ever, a NCC retracted its apical tail while leaving behind adherens junction parts, suggesting that the cell generated plenty of push to shear its tail while adherens junctions were undamaged at the separated apical tip (Fig. 1A.