Comparison of ganglioside profiles in nuclei and whole cells of NG108-15 and NG-CR72 lines: changes in response to different neuritogenic stimuli.
The plasma and nuclear membranes of neural cells have been shown to express gangliosides to a limited extent before, and at increasing levels during, differentiation. Recent studies employing qualitative cytochemistry have shown that GM1 expression in particular is significantly elevated in both membranes by specific neuritogenic agents. The present study provides a more complete description of ganglioside patterns of the 2 membranes of NG108-15 cells and a mutated form of the latter lacking gangliotetraose gangliosides. Nuclei of wild type NG108-15 cells were found to contain predominantly GM1 and GD1a, whereas whole cells had those in addition to substantial amounts of GM2 and GM3. GM1 and GD1a levels increased 2--3.5-fold in both whole cells and nuclei following axonogenic stimulation, but changed little in response to dendritogenic agents. GM2 expression, limited to the plasma membrane, showed little if any change with axonogenic stimuli but a 1.5--2-fold increase following treatment with dendritogenic agents. GM3 resembled GM2 in being virtually absent from the nuclear membrane, while its presence in the plasma membrane showed only modest change at most with any of the stimuli. The gangliotetraose ganglioside-deficient mutant cell line, NG-CR72, had significantly higher basal levels of GM2 in the plasma membrane compared to wild type NG108-15 cells, and this level increased significantly on treatment with dendritogenic agents. Basal GM3 levels were greatly reduced in the mutant cells and changed little with any of the stimuli. As expected, nuclei of NG-CR72 cells were virtually devoid of gangliosides. These mutant cells were previously shown to extend well defined dendritic neurites but were incapable of forming stable axonal processes. This study thus demonstrates major differences in the ganglioside content of wild type and mutated NG108-15 cells and their nuclei, and in their response to different neuritogenic stimuli.
Wu
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Department of Neurosciences, New Jersey Medical School, UMDNJ 185 South Orange Ave., Newark, NJ 07103, USA.
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Xie
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Ledeen
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D000818:Animals; D001369:Axons / Q000187:drug effects; D003994:Bucladesine / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism; D002467:Cell Nucleus / Q000737:chemistry / Q000378:metabolism*; D003712:Dendrites / Q000187:drug effects; D005732:Gangliosides / Q000032:analysis / Q000378:metabolism*; D015759:Ionomycin / Q000494:pharmacology; D051379:Mice; D009154:Mutation; D016501:Neurites / Q000187:drug effects / Q000378:metabolism*; D009447:Neuroblastoma / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D009685:Nuclear Envelope / Q000737:chemistry / Q000378:metabolism; D009844:Oligosaccharides / Q000172:deficiency / Q000235:genetics; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D014212:Tretinoin / Q000494:pharmacology; D014407:Tumor Cells, Cultured
D005732:Gangliosides; D009844:Oligosaccharides; D015759:Ionomycin; D014212:Tretinoin; D003994:Bucladesine; D011189:Potassium Chloride; C099478:gangliotetraose