Reactivity of normal and brachypod mouse limb mesenchymal cells with con A.

Abstract

SINCE plant lectins, such as concanavalin A (con A) and wheat germ agglutinin (WGA), bind to specific carbohydrate residues1, they have been used to investigate changes in plasma membranes during the course of normal development by monitoring lectin-induced agglutinability2–6, the binding affinities of carbohydrate moieties of cell-surface components for radioactively-Iabelled lectins2,5,6, and the distribution of binding sites using fluorescently conjugated lectins7. It has been proposed that agglutinability with con A and WGA varies with the stage of differentiation of a particular cell type1,2,5,6,8. It seems reasonable to assume, therefore, that modifications of cell-surface structure, such as changes in carbohydrate components or in their distribution on or in the plasma membranes, could result in the manifestation of an aberrant phenotype. Support for this notion comes from studies in which a reduced affinity for insulin and various plant lectins by liver cell plasma membranes was observed in young, hyperglycaemic mice9. Several studies on hereditary skeletal disorders10–12 including brachypodism (bpH) in mice13,14 have suggested that these anomalies originate at a time when the surface-mediated events of cell recognition and sorting-out are resulting in the formation of prechondrogenic blastemata15. Since rudiments derived from the postaxial region of the hind-limbs are the most severely affected in branchypodism13,14 con A agglutination and binding experiments were carried out on mesenchyme cells from this region in both normal (+/+) and mutant (bpH/bpH) embryos during early limb development. The results presented here show that differences occur over the 3-d test period supporting the contention that plasma membrane surfaces change during developments1–6,8. These developmental modifications are, however, temporally different between the two genotypically different cells which may be related to the ultimate manifestation of the abnormal phenotype.