Although numerous in vitro experiments suggest that extracellular matrix molecules like laminin can influence neural crest migration, little is known about their function in the embryo. Here, we show that laminin α5, a gene up-regulated during neural crest induction, is localized in regions of newly formed cranial and trunk neural folds and adjacent neural crest migratory pathways in a manner largely conserved between chick and mouse. In laminin α5 mutant mice, neural crest migratory streams appear expanded in width compared to wild type. Conversely, neural folds exposed to laminin α5 in vitro show a reduction by half in the number of migratory neural crest cells. During gangliogenesis, laminin α5 mutants exhibit defects in condensing cranial sensory and trunk sympathetic ganglia. However, ganglia apparently recover at later stages. These data suggest that the laminin α5 subunit functions as a cue that restricts neural crest cells, focusing their migratory pathways and condensation into ganglia. Thus, it is required for proper migration and timely differentiation of some neural crest populations.
Bibliographical noteFunding Information:
This work was supported by grants from the American Heart Association (0525037Y to E.G.C.) and NIH (DE15309 to L.S.G. and NS051051 to M.B.F.). We would like to thank David Anderson for the mouse NeuroD probe, Kirsten Kuhlbrodt and Michael Wegner for the mouse Sox10 , Lou Reichardt for the anti-p75 antibody, Peter Lwigale for the critical reading of the manuscript and Joaquin Gutierrez for the excellent animal husbandry.
- Cell migration
- Extracellular matrix
- Neural crest