Abstract

The Polymorphic expression of GM4(NeuAc), GM2(NeuGc), and GM1(NeuGc). Ganglisoide analysis of the progeny obtained on mating between BALB/C mice [GM4 (+)] and WHT/Ht or C57BL/6mice [both GM4(–)] indicated that the expression of GM 4(NeuAc) is an autosomal dominat trait, and that WHT/Ht and C67BL/6 mice carry a defect on a single autosomal gene. We named this gene Gsl–4. On quantitative determination of galactosylceramice (Galcer), which is the bisoynthetic precursor of GM4 (NeuAc), the content of GalCer was found to be quite low in WHT/Ht everythrocytes, compared with in BALB/c Erythrocytes. On analysis of GM4(Neu Ac) and Galcer in 92 back cross mice produced on mating between BALB/c and WHT/Ht mice, it was found that 45 GM4(+) mice apparently expressed a detectable amount of Galcer and that 47 GM4 (–) mice expressed an almost undetectable amount of Galcer. These results suggest the Gsl–4 controls the expression of GM4(NeuAc) by regulating the content of Galcer. Linkage analysis of Gsl–4 and the gene controlling GM2(NeuGc) in erythrocytes indicated that the two genes are not genetically linked. Comparison of the ganglioside expression in liver and erythrocytes of the same backcross mice suggested that the gene controlling GM2(NeuGc) expression in the liver (Ggm–2) is also responsible for the expression of CM2(NeuGc) in erythrocytes.

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