Differentiation-associated changes of glycolipid composition and metabolism in mouse myeloid leukemia cells. Induction of globotriaosylceramide and a galactosyltransferase.
This study was to find out whether induction of special glycolipids or glycosyltransferases for glycolipid synthesis which might be involved in the cell functions occurred during the differentiation. Mouse myeloid leukemia cell line (M1-), the differentiated cells (M1+), and a subcloned cell line ( Mm1) were used for this purpose. Gangliotriaosylceramide (GA2) was the major glycolipid component in M1- cells. As a result of differentiation of M1- into M1+ cells, globotriaosylceramide (CTH) was newly induced as the main glycolipid, while GA2 decreased to a minor component. GA2 was found to be the main glycolipid in Mm1 cells but no CTH was recognized. All precursor glycolipids and glycosyltransferases required to complete the biosynthetic pathway glucosylceramide (CMH) leads to lactosylceramide ( CDH) leads to GA2 leads to gangliotetraosylceramide (GA1) leads to sialosylgangliotetraosylceramide (GM1b) were found in M1- and also in Mm1 cells. A galactosyltransferase activity for CTH synthesis from CDH increased 10 fold during the differentiation. The induction of CTH in M1+ cells could be attributed to the increase of the galactosyltransferase activity. Both CTH as a surface marker and the galactosyltransferase as an enzyme marker are proposed as valuable markers of differentiation in M1- cells. Besides the galactosyltransferase, N-acetylglucosaminyltransferease involved in the formation of lactotriaosylceramide (amino-CTH) increased up to 3 fold during the differentiation. The increase of the enzyme activity seemed to be responsible for the biosynthesis of lactoneotetraosylceramide (paragloboside) which appeared in M1+ cells.[1]References
- Differentiation-associated changes of glycolipid composition and metabolism in mouse myeloid leukemia cells. Induction of globotriaosylceramide and a galactosyltransferase. Taki, T., Kawamoto, M., Seto, H., Noro, N., Masuda, T., Kannagi, R., Matsumoto, M. J. Biochem. (1983) [Pubmed]
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