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Modulation of cell competence for induction of differentiation in myeloid leukemic cells

It is shown that the competence of differentiation‐defective clones of mouse myeloid leukemic cells (MGI−D− clones) to be induced for some differentiation‐associated properties can be modulated. For certain inducers this was effected by changing the type of serum and for another inducer by removing serum from the culture medium. All the clones which could not be induced to differentiate by the differentiation‐inducing from of the normal macrophage and granulocyte inducing proteins MGI (MGI‐2), lipopolysaccharide (LPS), or dexamethasone (Dex) in serum‐free medium or in medium with horse, calf, rabbit, or sheep serum (nonpermissive serum) could be induced, by all three inducers, for the differentiation‐associated properties of lysozyme and Fc and/or C3 rosettes in syngeneic or allogeneic mouse serum or rat serum (permissive serum). The competence for induction of differentiation was altered merely by washing the cells and changing the type of serum, and addition of nonpermissive serum blocked the induction in permissive serum. This increased competence was associated with an increase in the ability for cap formation by concanavalin A. Removal of serum allowed some MGI−D− clones to be induced for lysozyme, Fc, and C3 rosettes by insulin. However, neither the changes in type of serum nor the removal of serum modulated in these clones the inducing effect of the tumor promoter 12‐O‐tetradecanoylphorbol‐13‐acetate. In contrast to the MGI−D− clones, changing the serum type or removing the serum did not modulate inducibility by MGI‐2, LPS, Dex, or insulin in other clones of myeloid leukemic cells that could be induced by MGI‐2 to differentiate either partly (MGI+D− clones) or completely (MGI+D+ clones) in horse or calf serum. The results indicate that by the appropriate modulation all MGI−D− clones tested could be induced for some differentiation‐associated properties; that there are factor(s) present in permissive sera which allow MGI−D− clones to be induced by MGI‐2, LPS, and Dex; that there are other factor(s) in nonpermissive sera which block this induction; and that in serum‐free medium cells of the appropriate clone can become susceptible to induction of these properties by insulin.