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Pathfinding by the trunk neural crest: the smart cell scenario.
Author(s) -
Erickson Carol A
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a89-a
Subject(s) - neural crest , biology , ephrin , neural tube , neuroscience , neural fold , erythropoietin producing hepatocellular (eph) receptor , anatomy , ectoderm , neural plate , microbiology and biotechnology , embryo , embryogenesis , signal transduction , receptor tyrosine kinase
Trunk neural crest cells migrate from the dorsal neural tube and produce the neurons and glial cells of the peripheral nervous system and the pigment cells of the skin. Although the neural crest cells are generally believed to be multipotent, we and others have recently discovered that neural crest cells are often lineage‐restricted when they leave the neural tube. The first neural crest cells to emigrate are the neuron and glial cell precursors, followed 12–18 hours later by melanoblasts. Aside from determining how the various neural crest lineages will differentiate, this early specification also controls what pathways the neural crest lineages will take. Neural and glial lineages can only migrate ventrally where the peripheral nervous system forms, whereas melanoblasts are uniquely able to take the dorsolateral path between the ectoderm and dermatome, where they will differentiate into the pigment cells of the skin. This ability to take different pathways is dependent upon their response to ephrins in the environment. Cells adhere to ephrins by way of the Eph receptors on their surface, and generally this interaction results in the cessation of migration. We have found that ephrins fill the dorsolateral pathway, and because the early migrating neuronal and glial precursors are inhibited by the ephrins, they migrate ventrally. However, melanoblasts are stimulated to migrate when they bind ephrins, and so they can invade the dorsolateral path. Our recent evidence suggests that pathfinding at the vagal level is also controlled by prior specification of some sublineages of the neural crest. In my talk I will consider how the mechanisms of pathway choice at the vagal level represent the transition between cell behavior in the head and the trunk, and why cell‐autonomous migratory behavior evolved for the crest cells taking the dorsolateral pathway.