c-myc and c-myb Oncoproteins During Induced Maturation of

c-myc and c-myb mRNA have been found to be tightly regulated during haemopoietic differentiation [1]. While the expression of both oncogenes is in-duced in cells stimulated to proliferate, c-myc in the transition from Go to G 1 [2], and c-myb in the transition from G 1 to S phase [3], expression ceases in terminally differentiating haemopoietic cell lines. This takes the form of a progressive monotonic mRNA decline during macrophage (Mel') and granulocyte (GN) differentiation and a biphasic mRNA decline during erythroid (E) dif-ferentiation [4-6]. Although this decline may reflect the cessation of proliferation which accompanies the differentiation process, recent reports that constitutive expression of either oncogene inhibits differentiation in murine [7] and human [8] leukaemic lines imply a causative role for each in haemopoietic maturation. We have studied nuclear c-myc and c-myb proteins through the cell cycle dur-ing Mel', GN, E and megakaryocytic (MK) differentiation of KG1, HL60 and HEL leukaemic cells. The p62c-myc and p75c-myb content of propidium-iodide stained nuclei was quantitated by flow cytometry using fluoresceinated antibod-ies CT14-G4 and MB4.3, respectively (gifts of G. Evan, Cambridge, UK), fol-lowing our published method [9]. Figure 1 is a dot display ofp62c-myc and p75c-mcb fluorescence in uninduced HL60, demonstrating a less than two-fold incre-ment in both oncoproteins over the cell cycle