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Surface functions during mitosis in rat basophilic leukemia cells.
The Journal of Cell Biology
|December 1, 1985
Summary
Mitotic cells retain surface receptors but lose functional responses like serotonin release and fluid pinocytosis, indicating a failure in transmembrane signaling during mitosis.
Area of Science:
- Cell Biology
- Immunology
- Molecular Biology
Background:
- Cells lose membrane activities like phagocytosis upon entering mitosis.
- Mitotic cells exhibit resistance to functional responses triggered by cell surface ligand-receptor interactions.
Purpose of the Study:
- To investigate whether mitotic cells resist functional responses to cell surface ligand-receptor interactions.
- To determine the impact of mitosis on IgE receptor-mediated signaling and cell surface dynamics.
Main Methods:
- Utilized RBL-2H3 rat basophilic leukemia cells labeled with anti-dinitrophenol IgE (anti-DNP-IgE).
- Cross-linked IgE receptors with multivalent ligands (DNP-bovine serum albumin [BSA], DNP-B-phycoerythrin, DNP-BSA-gold).
- Assessed [3H]serotonin release, cell surface topography changes, and fluid pinocytosis in interphase versus mitotic cells.
Main Results:
- IgE-receptor complexes remained on the cell surface throughout mitosis, binding ligands and redistributing to coated pits.
- Antigen stimulation failed to induce significant [3H]serotonin release in mitotic cells.
- Mitotic cells maintained a microvillous surface and ceased fluid pinocytosis, unlike interphase cells.
Conclusions:
- Mitosis-specific impairment of membrane and secretory responses is likely caused by a failure in transmembrane signaling.
- Cell surface receptor-ligand interactions are functionally suppressed during mitosis.
- Protein kinase C activation can restore some membrane activities in mitotic cells.