The proliferating field of neural crest stem cells.

Neural crest stem cells were first isolated from early embryonic neural crest in the early 1990s, but in the past 5 years, there has been a burst of discoveries of neural crest-derived stem cells from diverse locations. Here, we summarize these data, highlighting the characteristics of each stem cell type. These cells vary widely in the markers they express and the variety of cell types they appear to generate. They occupy diverse locations, but in some cases multiple stem cell types apparently occupy physically proximate niches. To date, few molecular similarities can be identified between these stem cells, although a systematic comparison is required. We note other issues worthy of attention, including aspects of the in vivo behavior of these stem cells, their niches, and their lineage relationships. Together, analysis of these issues will clarify this expanding, but still young, field and contribute to exploration of the important therapeutic potential of these cells.

Sdf1a patterns zebrafish melanophores and links the somite and melanophore pattern defects in choker mutants.

Pigment pattern formation in zebrafish presents a tractable model system for studying the morphogenesis of neural crest derivatives. Embryos mutant for choker manifest a unique pigment pattern phenotype that combines a loss of lateral stripe melanophores with an ectopic melanophore ;collar' at the head-trunk border. We find that defects in neural crest migration are largely restricted to the lateral migration pathway, affecting both xanthophores (lost) and melanophores (gained) in choker mutants. Double mutant and timelapse analyses demonstrate that these defects are likely to be driven independently, the collar being formed by invasion of melanophores from the dorsal and ventral stripes. Using tissue transplantation, we show that melanophore patterning depends upon the underlying somitic cells, the myotomal derivatives of which--both slow--and fast-twitch muscle fibres--are themselves significantly disorganised in the region of the ectopic collar. In addition, we uncover an aberrant pattern of expression of the gene encoding the chemokine Sdf1a in choker mutant homozygotes that correlates with each aspect of the melanophore pattern defect. Using morpholino knock-down and ectopic expression experiments, we provide evidence to suggest that Sdf1a drives melanophore invasion in the choker mutant collar and normally plays an essential role in patterning the lateral stripe. We thus identify Sdf1 as a key molecule in pigment pattern formation, adding to the growing inventory of its roles in embryonic development.