At the entry into mitosis, cells abruptly lose membrane activities such as phagocytosis, pinocytosis, and capping. The present studies test if mitotic cells also resist functional responses to cell surface
ligand-receptor interactions. The
IgE receptors of RBL-2H3 rat basophilic
leukemia cells were labeled with anti-dinitrophenol
IgE (anti-DNP-
IgE) and then cross-linked with multivalent
ligands (DNP-
bovine serum albumin [BSA]; DNP-B-
phycoerythrin;
DNP-BSA-
gold).
IgE-receptor cross-linking modulates cell surface organization and function and releases
serotonin and other mediators of allergic and asthmatic reactions from interphase cells (Pfeiffer, J. R., JC. Seagrave, B. H. Davis, G. G. Deanin, and J. M. Oliver, 1985, J. Cell Biol., 101:2145-2155). It was found that anti-DNP-
IgE-receptor complexes are preserved on the cell surface throughout mitosis; they continue to bind DNP-
proteins, and the resulting
antigen-
IgE-receptor complexes can redistribute to coated pits on the cell surface. Furthermore, there is no loss of [3H]
serotonin through mitosis. Nevertheless,
antigen-stimulated [3H]-
serotonin release is strongly impaired in mitotic-enriched as compared with mixed interphase or G1-enriched cell populations. In addition,
antigen binding transforms the surface of interphase cells from a microvillous to a plicated topography and stimulates the uptake of
fluorescein isothiocyanate-conjugated
dextran by fluid pinocytosis. Mitotic cells maintain a microvillous surface topography after
antigen treatment, and fluid pinocytosis virtually ceases from prometaphase to telophase.
Phorbol myristate acetate, a
tumor promoter that activates
protein kinase C, restores surface ruffling activity to mitotic cells. Thus, the mitosis-specific freezing of membrane and secretory responses is most likely due to the failure of transmembrane signaling.