Introduction Cell migration during morphogenesis and organogenesis is under strict spatial and temporal control. Several lines of evidence suggest that migration is regulated by interactions

Cell migration during morphogenesis and organogenesis is under strict spatial and temporal control. Several lines of evidence suggest that migration is regulated by interactions of cells with the extracellular matrix (ECM) (see reviews by Thiery, 1985; Bronner-Fraser, 1990; Johnson et al., 1990). These interactions take place between cell surface receptors and their ECM ligands, among which fibronectin has been shown to be of major importance (Yamada, 1983). In vitro, fibronectin promotes cell migration (Ali and Hynes, 1978; Heasman et al., 1981; Rovasio et al., 1983; Shi et al., 1989) and it is required in vivo for mesodermal cell migration during amphibian gastrulation as well as for avian neural crest cell migration (Boucaut et al., 1984a,b; Bronner-Fraser, 1985, 1986; Darribère et al., 1988, 1990; Poole and Thiery, 1986). Because of the widespread distribution of fibronectin during development, attention has recently turned to ECM-components which interfere with cell-adhesion to fibronectin and therefore might act to guide migrating cells along the correct pathways (Perris and Johansson, 1987; Chiquet-Ehrismann et al., 1988; Hoffman et al., 1988). Tenascin (TN, Chiquet and Fambrough, 1984 a,b; Chiquet-Ehrismann et al., 1986), also called cytotactin (Grumet et al., 1985), has been shown to inhibit adhesion in vitro to purified fibronectin-substrata (Tan et al., 1987; ChiquetEhrismann et al., 1988; Halfter et al., 1989) and to inhibit 147 Development 116, 147-157 (1992) Printed in Great Britain © The Company of Biologists Limited 1992