The neural crest (NC) is a transient and migratory population of cells that gives rise to a variety of cell types. During development, NC cells delaminate from the neural tube in a process that is closely coordinated with the process of neural tube closure, and studies have shown that signalling via the planar cell polarity (PCP) pathway is essential for both of these processes in Xenopus and zebrafish. However, it is unclear if PCP signalling is required for NC migration in mammals. Here, Andrew Copp and colleagues address this issue (p. 3153). They show that NC specification, migration and tissue colonisation are not perturbed in mice that lack the function of the core PCP protein Vangl2. Furthermore, they demonstrate that Vangl1 does not compensate for the loss of Vangl2, as Vangl1/Vangl2 double-mutant mice also exhibit normal NC migration. The NC-specific ablation of Vangl2 activity also has no effect on NC migration. Finally, the researchers demonstrate that the migratory properties of NC cells from wild-type and Vangl2 mutant neural tube explants cultured in vitro are indistinguishable. Together, these findings confirm that, in contrast to its essential role in neural tube closure, PCP signalling is not essential for NC migration. Importantly, these findings also suggest that PCP mutations are unlikely to be the cause of NC-related birth defects in humans.
PCP signalling is dispensable for neural crest migration
PCP signalling is dispensable for neural crest migration. Development 15 August 2014; 141 (16): e1601. doi:
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