An Antibody to a Receptor for Fibronectin and Laminin Perturbs Cranial Neural Crest Development in Vivo

Abstract

Previous studies from this laboratory (M. Bronner-Fraser (1985). J. Cell Biol. 101, 610) have demonstrated that an antibody to a cell surface receptor complex caused alternations in avian neural crest cell migration. Here, these observations are extended to examine the distribution and persistency of injected antibody, the dose dependency of the effect, and the long-term influences of antibody injection. The CSAT antibody, which recognizes a cell surface receptor for fibronectin and laminin, was injected lateral to the mesencephalic neural tube at the onset of cranial neural crest migration. Injected antibody molecules did not cross the midline, but appeared to diffuse throughout the injected half of the mesencephalon, where they remained detectable by immunocytochemistry for about 22 hr. Embryos were examined either during neural crest migration (up to 24 hr after injection) or after formation of neural crest-derived structures (36–48 hr after injection). In those embryo fixed within the first 24 hr, the major defects were a reduction in the neural crest cell number on the injected side, a buildup of neural crest cells within the lumen of the neural tube, and ectopically localized neural crest cells. In embryos allowed to survive for 36 to 48 hr after injection, the neural crest derivatives appeared normal on both the injected and control side, suggesting that the embryos compensated for the reduction in neural crest cell number on the injected side. However, the embryos often had severely deformed neural tubes and ectopic aggregates of neural crest cells. In contrast, several control antibodies had no effect. These findings suggest that the CSAT receptor complex is important in the normal development of the neural crest and neural tube.

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