Distribution of immunoglobulin on the surface of mouse lymphoid cells as determined by immunoferritin electron microscopy, Antibody‐induced, temperature‐dependent redistribution and its implications for membrane structure

Abstract

The ultrastructural distribution of membrane-bound immunoglobulin (Ig) on mouse spleen lymphocytes has been studied by labeling the surface Ig with anti-mouse Ig antibody conjugated t o ferritin (FT). The distribution is temperature-dependent. At 0 OC -4 OC FTzppears p t r i b u t e d in small clusters over the entire surface, whereas at 2 0 C -22 C, in the great majority of the labeled cells, it is concentrated over one pole. This pole corresponds t o that part of the cell which contains the G o l d complex and most of the cellular organelles, and which forms the uropod in moving lymphocytes. This polar redistribution is accompanied by endocytosis of part of the labeled membrane.The redistribution of label occurring at room temperature indicates that labeled and unlabeled components of the plasma membrane can segregate from each other and suggests that plasma membrane is fluid at room temperature. The diffuse distribution found at 0 OC -4 OC is probably close (although not identical) t o the distribution in vivo before labeling, while the polar distribution at higher temperature is probably induced by the cross-linking of the surface Ig molecules by the antibody-FT conjugate and by a metabolically-dependent flow of the aggregates towards the "tail" of the lymphocyte. The mechanism involved is considered to be the same mechanism responsible for membrane flow during cell movement. A detailed model of the structure and rheological properties of the lymphocyte membrane is proposed, which can explain the present results and those of others concerning the behavior of surface components of lymphocytes and other cells.

Cholera toxin mediated activation of adenylate cyclase in intact rat hepatocytes

“…Such patching and capping of fluorescent cholera toxin [19,20] also patches and caps the GM,, gangliosides [21] indicating that it is this entire complex which is redistributed in the plane of the membrane. The change in the lag period with cholera toxin concentration in intact hepatocytes will thus reflect the amount of toxin bound and undoubtedly the effi- Patching and capping phenomena are known to be temperature dependent [22], and are presumably dependent upon bilayer fluidity. Indeed a fluid bilayer is a pre-requisite for patch formation due to the interaction of a multivalent ganglioside complex [4] with mutlivalent receptors which aggregate by free lateral diffusion in the plane of the bilayer, to be subsequently removed to a pole of the cell to form a cap.…”

Spontaneous internalization of Class I major histocompatibility complex molecules in T lymphoid cells.

“…On the whole, the process of MHC internalization in activated lymphoid cells resembles more closely the spontaneous internalization of other receptors as seen in different kinds of cells, such as the low density lipoprotein (LDL) receptor in fibroblasts (24), the asialoglycoprotein receptor in hepatic cells, (25) or the receptor for transferrin in fibroblasts (26) and in lymphoblasts, (27) than the internalization of membrane immunoglobulins in B lymphoid cells, which never occurs spontaneously and is instead strictly dependent upon interaction with a cross-linking ligand (28).…”

Actin associated with purified lymphocyte plasma membrane

“…microfilaments) and monomeric form, has, however, yet to be clearly defined. In the case of lymphocytes, microfilaments have been implicated in various cell surface-mediated phenomena including the capping of surface immunoglobulin [2][3][4][5], lectin-induced mitogenicity [6,7] and lymphocyte-mediated cytotoxicity [8,9]. One possible explanation for the apparent linkage between cell surface events and cytoplasmic microfilaments would be a specific interaction between the filaments and the cell surface (plasma) membrane.…”