Mechanisms of neural crest cell migration

Abstract

Neural crest cells are remarkable in their extensive and stereotypic patterns of migration. The pathways of neural crest migration have been documented by cell marking techniques, including interspecific neural tube grafts, immunocytochemistry and DiI-labelling. In the trunk, neural crest cells migrate dorsally under the skin or ventrally through the somites, where they move in a segmental fashion through the rostral half of each sclerotome. The segmental migration of neural crest cells appears to be prescribed by the somites, perhaps by an inhibitory cue from the caudal half. Within the rostral sclerotome, neural crest cells fill the available space except for a region around the notochord, suggesting the notochord may inhibit neural crest cells in its vicinity. In the cranial region, antibody perturbation experiments suggest that multiple cell-matrix interactions are required for proper in vivo migration of neural crest cells. Neural crest cells utilize integrin receptors to bind to a number of extracellular matrix molecules. Substrate selective inhibition of neural crest cell attachment in vitro by integrin antibodies and antisense oligonucleotides has demonstrated that they possess at least three integrins, one being an alpha 1 beta 1 integrin which functions in the absence of divalent cations. Thus, neural crest cells utilize complex sets of interactions which may differ at different axial levels.

Regulation of neural progenitor proliferation and survival by β1 integrins

“…Migration of neurosphere-derived mutant cells is significantly decreased on both laminin-1 and fibronectin substrates Integrins also regulate the migration of several cell types both in vitro (Jacques et al, 1998;Milner et al, 1996) and in vivo (Bronner-Fraser, 1993;Galileo et al, 1992). To determine if the loss of β1 integrin could alter the migration capacities of cells derived from mutant and control neurospheres, we measured the extent of cell migration from intact neurospheres plated on PDL, laminin-1 and fibronectin substrates, in the absence or presence of growth factors (3.3 ng/ml EGF, 2.0 ng/ml FGF, 10 ng/ml NGF) (Ohtsuka et al, 2001).…”

A novel role for MuSK and non-canonical Wnt signaling during segmental neural crest cell migration

“…A novel role for MuSK in neural crest cell migration Elegant manipulations have shown that neural crest cells enter two broad migration routes known as the dorsolateral and ventromedial pathways (Bronner-Fraser, 1993). A unique feature of the ventromedial pathway is that neural crest cells entering this route rearrange from a continuous sheet into narrow, segmentally restricted streams.…”

The temporal sequence of spontaneous repair of osteochondral defects in the knees of rabbits is dependent on the geometry of the defect

“…Therefore it seems that as the clot is stretched over a larger area the cells adherent to this clot are stretched in the same plane and this dictates their later shape and surrounding extracellular matrix. [20][21][22][23] The smaller defects repair with initially more metachromatic staining but the lack of subchondral support in the smaller defects seems to lead to an earlier breakdown of the cartilage layer. We also noted a lack of interdigitation of the collagen fibres with time at the interface between the reparative tissue and the adjacent host cartilage.…”

“…They were then returned to their cages and allowed intermittent active mobilisation. 19 On various days after surgery (3,7,14,21,28,42,84 and 126) eight rabbits were killed with carbon dioxide. The knee was dissected and the distal femur fixed in 10% phosphate-buffered formalin for at least 48 hours before staining.…”