Fibronectin, mesoderm migration, and gastrulation in Xenopus.
The role of fibronectin in mesoderm cell migration and and the importance of mesoderm migration for gastrulation in Xenopus are examined. To allow for migration, a stable interface must exist between migrating mesoderm cells and the cells of the substrate layer, the blastocoel roof. We show that maintenance of this interface does not depend on fibronectin. We further demonstrate that fibronectin contributes to, but is not essential for, mesoderm cell adhesion to the blastocoel roof. However, interaction with fibronectin is necessary for cell spreading and the formation of lamelliform cytoplasmic protrusions. Apparently, the specific role of fibronectin in mesoderm migration is to control cell protrusive activity. Consequently, when fibronectin function is blocked by GRGDSP peptide or antibodies, mesoderm cell migration is inhibited. Nevertheless, gastrulation proceeds nearly normally in inhibitor-treated embryos. It appears that in Xenopus, mesoderm migration is not essential for gastrulation.
Winklbauer
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R
Department of Zoology, University of California, Berkeley 94720, USA. rwinkl@novell.biolan.uni-koeln.de
Keller
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RE
D000818:Animals; D001755:Blastocyst / Q000502:physiology; D002448:Cell Adhesion; D002465:Cell Movement / Q000502:physiology*; D004625:Embryo, Nonmammalian / Q000196:embryology; D005353:Fibronectins / Q000502:physiology*; D005775:Gastrula / Q000502:physiology*; D008648:Mesoderm / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D008855:Microscopy, Electron, Scanning; D014982:Xenopus laevis / Q000196:embryology*
D005353:Fibronectins