The tumour suppressor p53 plays multiple roles in the prevention of cancer but its developmental functions are less clear. Here (see p. ), Eldad Tzahor and colleagues elucidate the key role that p53 plays in craniofacial development. During embryogenesis, cranial neural crest (CNC) cells give rise to the facial bones, cartilage and connective tissues. Neural crest development involves an epithelial-mesenchymal transition (EMT) that converts epithelial cells into migratory mesenchymal cells, which delaminate from the neural tube. Notably, EMT is an early step in tumour progression. The researchers report that craniofacial development is disrupted in p53 knockout mouse embryos. Then, they show that p53 is expressed in CNC progenitors in chick embryos but that its expression decreases as these cells delaminate from the neural tube. Moreover, p53 gain-of-function results in fewer migrating CNC cells, whereas p53 loss-of-function increases the EMT/delamination of CNC cells. These and other findings suggest that p53 coordinates CNC growth and EMT/delamination processes during craniofacial development.
