Abstract
The inherent topographical distribution of Con A binding sites (CABS) is disperse or random in all cell types studied using hemocyanin to mark CABS in surface replicas. In virally transformed cells, the addition of Con A leads to the formation of clusters (CABS). A role for microtubules is suggested in this process since colchicine treatment of transformed cells and Con A addition lead to the aggregation of Con A into a “cap.” During phagocytosis CABS are selectively removed from the surface. This selective movement is abolished by drugs that disrupt microtubules. Binding of Con A or RCA to intact cells at 37°C leads to the removal of their receptors from the surface, presumably by “micropinocytosis.”