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Ganglioside Composition of Normal and Mutant Mouse Embryos
Author(s) -
Bouvier Joseph D.,
Seyfried Thomas N.
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb09143.x
Subject(s) - ganglioside , neural tube , sialic acid , mutant , biology , embryo , microbiology and biotechnology , biochemistry , endocrinology , gene
The enrichment of gangliosides in neuronal membranes suggests that they play an important role in CNS development. We recently found a marked tetrasialoganglioside deficiency in t w1 /t w1 mutant mouse embryos at embryonic day (E)‐11. The recessive t w1 /t w1 mutants die at embryonic ages E‐9 to E‐18 from failed neural differentiation in the ventral portion of the neural tube. In the present study, we examined the composition and distribution of gangliosides in t w1 /t w1 mutant mouse embryos at E‐12. The total ganglioside sialic acid concentration was significantly lower in the mutants than in normal (+/‐) embryos. The mutants also expressed significant deficiencies of gangliosides in the “b′’ metabolic pathway (GD3, GD1b, GT1b, and GQ1b) and elevations in levels of gangliosides in the “a′’ metabolic pathway (GM3, GM2, GM1, and GD1a). These findings suggest that the mutants have a partial deficiency in the activity of a specific sialyltransferase in the b pathway. Regional ganglioside distribution was also studied in E‐12 normal mouse embryos. The ganglioside composition in heads and bodies was similar to each other and to whole embryos. Total ganglioside concentration and the distribution of b pathway gangliosides were significantly higher in neural tube regions than in nonneural tube regions. These findings suggest that b pathway gangliosides accumulate in differentiating neural cells and that the deficiency of these gangliosides in the t w1 /t w1 mutants is closely associated with failed neural differentiation.