Neural Crest Development

Abstract

Neural crest arises at the interface of the ectoderm and neural tissue via inductive interactions between the two tissues (Fig. 8; Rosenquist 1981; Moury and Jacobson 1990; Selleck and Bronner-Fraser 1995; Mancilla and Mayor 1996). In fact, placement of the ectoderm and the neural plate together in in vivo or in vitro recombination assays can induce neural crest formation with neural crest cells forming from both the ectoderm and neural tissue (reviewed by Selleck and Bronner-Fraser 1996; LaBonne and Bronner-Fraser 1999). Most of these studies have been carried out in the trunk, but the tissue interactions that control cranial neural crest formation are likely to be similar if not identical. However, as recently shown by the studies of the effect of slug overexpression in the developing trunk and cranial regions, the molecular mechanisms of neural crest generation are not exactly identical (del Barrio and Nieto 2002). These molecular differences are also emphasised by the differential expression of genes such as the hyaluronan receptor, CD44, and the transcription factor, Id2, which are restricted to the cranial neural crest (Martinsen and Bronner-Fraser 1998; Corbel et al. 2000; also see Sect. 4.3 and the review by Nieto 2001). In chicks, the neural/epithelial boundary, which gives rise to the neural crest precursors, is set up by antagonistic interactions between Bmp and Fgf signalling in conjunction with a signal from the midline of the neural plate (Pera et al. 1999; Streit and Stern 1999). At this early stage, the presumptive neural crest cells are not specified and are competent to produce neural crest in addition to neuronal and ectodermal derivatives (Selleck and Bronner-Fraser 1995). Later, they become restricted to either a neural crest or neuronal fate.