Treatment of mouse teratocarcinoma F9 cells with all-trans-retinoic acid (RA) causes a 9-fold increase in steady-state levels of mRNA for UDP-Gal:-D-Gal 1,3-galactosyltransferase (1,3GT) beginning at 36 h. Enzyme activity rises in a similar fashion, which also parallels the induction of laminin and type IV collagen. Nuclear run-on assays indicate that this increase in 1,3GT in RA-treated F9 cells, like that of type IV collagen, is transcriptionally regulated. Differentiation also results in increased secretion of soluble 1,3GT activity into the growth media. The major -galactosylated glycoprotein present in the media of RA-treated F9 cells, but not of untreated cells, was identified as laminin. Differentiation of F9 cells is accompanied by an increase in -galactosylation of membrane glycoproteins and a decrease in expression of the stage-specific embryonic antigen, SSEA-1 (also known as the Lewis X antigen or Le), which has the structure Gal1-4(Fuc1-3)GlcNAc1-R. However, flow cytometric analyses with specific antibodies and lectins, following treatment of cells with -galactosidase, demonstrate that differentiated cells contain Le antigens that are masked by -galactosylation. Thus, RA induces 1,3GT at the transcriptional level, resulting in major alterations in the surface phenotype of the cells and masking of Le antigens.

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