Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells

Abstract

Exposure of F9 cells to all-trans-retinoic acid over a period of 6 days resulted in 4-fold induction of cell surface N-acetylglucosaminide fi( l -+4)galactosyltransferase (GT) activity. The retinoic acid-induced GT activity was further enhanced by treatment of the cells with I-bromo cyclic AMP. The ability of retinoic acid alone, or retinoic acid in combination with 8-bromo cyclic AMP, to induce GT activity was inhibited by both actinomycin D and cycloheximide. These findings indicate that the induction of galactosyltransferase activity noted with differentiation of F9 cells involves de novo synthesis of new enzyme protein. F9 cell Retinoic acid 8-Bromo cyclic AMP Galactosyltransferase activity De novo synthesis

Induction of major histocompatibility class I antigens by interferons in undifferentiated F9 cells

“…The materials (1 mg/ml, 6 x lo6 U/ml) were stored at 4°C and were diluted immediately before use. A mixture of mouse interferon-a and -p (IFN-dO) was purchased from Lee Biomolecular Research Inc. To induce in vitro differentiation, retinoic acid (0.1 pM), (Sigma and Eastman Kodak) with or without 8-Bromoadenosine 3'5'cyclic monophosphate (c-AMP) (0.1 mM, Sigma) was used (Strickland and Mahdavi, 1978;Strickland et al, 1980;Nakahashi et al, 1984). To block protein synthesis (Ringold et al, 1984), cycloheximide (CHX) (Sigma) was used diluted at 35 pglml in the medium.…”