Neural Crest Induction and Differentiation

Volume 589 of the series Advances in Experimental Medicine and Biology pp 32-44

Transcriptional Regulation at the Neural Plate Border

  • Thomas D. SargentAffiliated withLaboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health

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The neural crest (NC) is usually defined as a cell type arising at the border of the neural plate and the epidermis in vertebrate embryos. While accurate, this definition implies that the border exists as a distinct boundary, which is not really the case. Like other domains in the early embryo, the NC is not a sharply delimited territory, but rather is an overlapping zone of specification that has characteristics of both epidermis and neural plate, with additional characteristics of its own. This can be seen in the spatial pattern of regulatory factors that have been implicated in NC induction, many of which are shared.1 For example Msx1 and AP2 are also expressed in the epidermis, at lower levels, and c-myc is likewise transcribed in neural plate in addition to NC. Nor is this limited to regulatory factors. The epidermal keratins, which constitute the intermediate filament cytoskeleton of epidermal cells are also expressed in NC, at a lower level than the epidermis. This can be seen by in situ hybridization (Fig. 1A) as a region of relatively weak but significant signal in the cranial neural crest region. Another indication of the fuzzy nature of NC comes from lineage mapping experiments in the chick embryo, which show that cells fated to differentiate as NC, neural plate, epidermis and placodal derivatives are all intermingled in the neural-epidermal boundary region.2 Nor is there always a clear gap visible between neural plate and epidermal gene expression domains, for example in a double in situ with epidermal keratin and the pan-neural marker NCAM the two domains are contiguous (Fig. 1B). Expression of keratin genes is also evident in animal caps that have been dissected from embryos injected with BMP antagonists, such as chordin, along with a canonical Wnt signal molecule, such as Wnt3a.