Capping phenomena have been described for a variety of membrane components in a variety of cell types. The basic model remains the polar capping of membrane immunoglobulins (mlg) on B lymphocytes by anti-immunoglobulin antibody. When different membrane components are successively capped, they migrate to the same cell pole. This pole is assigned to the cell by the zone of contact of its membrane either with another cell or with a substratum. The general characteristics of the capping phenomenon, particularly the energy requirements, temperature dependence, inhibition or reversion by microfila-ment-directed drugs (cytochalasins), and the accumulation of microfilaments under the cap, have led to the suggestion that capping is probably an active cellular contractile phenomenon. Early cell adhesion studies also suggested that the expression, distribution and dynamics of ligand recognizing domains might be controled by the microfilamentous network of the cell. Ligand recognition may be followed by cell motility changes and by increased adhesion to a substratum or to other cells. As early as 1973, expression of adhesive sites by lymphocytes was also found to be an active cellular process, its linkage to microfilament dynamics being shown later. It is unclear, however, whether adhesion and capping may be mechanistically related to each other.

For capping to occur, contractile microfilaments drag anchored patches of aggregated membrane components into an area of the cell where they can be endocytosed and digested, or shed from the surface. As microtubules do not appear to enhance microfilament mobility but rather to inhibit it, their role in the capping phenomenon is more complex. When microtubules are depolymerized by exposing the cells to specific drugs (e.g. colchicine, Vinca alkaloids) or to a chilling shock, the capping occurs on the uropod of the cell. Shedding or endocytosis may, however, occur on the whole cell surface when microtubules interfere with the polar redistribution of clustered ligands and membrane components. Capping of any membrane component would occur as a consequence of entrapment of microfilament-

associated membrane anchors within the lattices or clusters formed on the plasma membrane. These microfilament-driven anchors would then sweep any aggregated membrane components or adsorbed material toward the cap area, a zone of high endocy-totic activity. Both the membrane sites involved in intercellular adhesion and the membrane anchors involved in capping might be proteins of the integrin and cadherin families.

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