Prevention of gastrulation but not neurulation by antibodies to fibronectin in amphibian embryos

Abstract

Gastrulation and formation of the neural plate are major steps in early vertebrate embryogenesis. Although morphogenetic movements leading to the formation of the primary germ layers have been extensively described^1–3, the mechanisms governing migration of mesodermal cells and their interactions with ectoderm remain ill-defined. A large body of evidence indicates that fibronectin (FN), a high molecular weight cell-surface-associated glycoprotein, promotes cell adhesion and cell migration throughout embryogenesis^4–6. FN has been detected at an early blastula stage in Pleurodeles waltlii⁷. We now show that FN is a component of a dense fibrillar matrix underlying the blastocoel roof; in contrast, the exterior surface of the embryo is devoid of FN. Microsurgical inversion of part of the blastocoel roof does not prevent mesodermal cell migration except at the site of inversion where no FN matrix is available. Perturbation experiments using antibodies to FN demonstrate that the invagination of presumptive mesodermal cells does not occur when the monovalent antibodies are injected before or at the onset of gastrulation; on the other hand, the formation of a neural plate is not prevented when late gastrula stage embryos are treated with antibodies to FN. We conclude that the presence of FN is required for cell migration during gastrulation.