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Review
. 1993 Dec;60(3):517-37.
doi: 10.1016/0163-7258(93)90034-b.

Adhesion molecules in neural crest development

Affiliations
Review

Adhesion molecules in neural crest development

D F Newgreen et al. Pharmacol Ther. 1993 Dec.

Abstract

Peripheral nerve cells, various endocrine and pigment cells and cranial connective tissue cells of vertebrates stem mainly from the embryonic neural crest. This originates with the central nervous system, but the crest cells detach from this tissue, via a decrease of cell-cell adhesion involving, particularly, a reduction of the adherens junction cell adhesive molecule A-CAM. This epithelio-mesenchymal transformation allows crest cells to migrate along pathways that are defined partly by the distribution of substrate adhesion molecules, the archetype being fibronectin, an extracellular matrix molecule recognized by integrin receptors on crest cells. Many other molecules, however, may act in the same way. In contrast, some molecules may define migration pathways by reducing adhesion; chondroitin sulfate proteoglycan is a candidate for this role. Pathway selection is most likely achieved by balanced combinations of molecules that promote and reduce adhesion. Cessation of migration, in the case of the nervous ganglia, correlated with re-expression of cell-cell adhesion molecules like A-CAM and others, consistent with an adhesive basis, although functional tests have not yet been performed. The development of the neural crest system provides a useful model that emphasizes the role of adhesion in morphogenesis.

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