Regulation of AMUGs and AMDGs by AML1b and AML1a.

(A) Differential display patterns of 6 cDNA fragments in control (LNSX and LNCX) and AML1-MTG8-, AML1b-, and AML1a-expressing L-G cells. AML1-MTG8 and AML1b were introduced on an LNSX vector by retrovirus infection, and AML1a was introduced on an LNCX vector. Control cells were infected with the respective mock vectors. Each fragment is indicated by an arrow. (B) Northern blotting analysis of the expression of 3 AMUGs and 3 AMDGs in control and AML1-MTG8-, AML1b-, and AML1a-expressing L-G cells. The membranes were hybridized with the corresponding cDNA fragments isolated by the differential display analysis. Human G3PDH cDNA was used as a control probe. The expression of B16G120, MRP14, and granzyme B was counterregulated by AML1b and AML1-MTG8. These genes were up- or down-regulated by AML1a as by AML1-MTG8. The expression of mast cell carboxypeptidase A, CD53, and Pim-2 was not altered by AML1b, but altered by AML1a as by AML1-MTG8. The AML1a-mediated alteration, even though faint as seen in the case ofmast cell carboxypeptidase A, was considered to reflect the competitive inhibition of endogenous AML1b-dependent transcription. The expression of TIS11b,β-galactoside-α2,6-syalyltransferase,and interferon-induced mRNA was specifically altered by AML1-MTG8 but not altered by either AML1b or AML1a.