Hapten inhibitors of the endogenous galactose binding lectins and anti-lectin antibodies inhibit primitive streak formation in the early chick embryo.

The early chick blastoderm expresses two endogenous galactose-binding lectins of 14 kDa and 16 kDa. We have studied the effect the lectin hapten inhibitors thiodigalactoside and the synthetic neoglycoprotein lactosyl-bovine serum albumin as well as polyclonal anti-lectin antibodies on the development of early chick embryos cultured in a defined medium. Controls consisted of maltose, maltosyl bovine serum albumin and rabbit IgG. Embryos treated at the onset of cell migration during early gastrulation underwent blastoderm retraction with decrease in surface area. In addition, they exhibited a lack of demarcation between the presumptive embryonic area (area pellucida) and the presumptive extraembryonic area (area opaca). These blastoderms also lacked a primitive streak, that is, the structure that forms in the area pellucida during gastrulation as cell migrate to form the endodermal and mesodermal layers of the embryo. Embryos treated at later stages of gastrulation showed development similar to that of controls in that they were able to undergo early organogenesis. The results suggest that lectin mediated mechanisms are essential for the migratory movements of early gastrulation and that, at late gastrulation, other mechanisms exist in the embryo to compensate for lectin function.