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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1578-1589
c-Maf Induces Monocytic Differentiation and Apoptosis in Bipotent
Myeloid Progenitors
Shrikanth P. Hegde,
JingFeng Zhao,
Richard A. Ashmun, and
Linda H. Shapiro
From the Departments of Pathology and Laboratory Medicine and
Tumor Cell Biology, St Jude Children's Research Hospital,
Memphis, TN.
The transcriptional mechanisms that drive colony-forming unit
granulocyte-macrophage (CFU-GM) myeloid progenitors to differentiate into cells of either the granulocytic or monocytic lineage are not
fully understood. We have shown that the c-Maf and c-Myb transcription factors physically interact in myeloid cells to form inhibitory complexes that hinder transactivation of c-Myb target genes through direct binding to Myb consensus sites. These complexes arise in a
developmentally regulated pattern, peaking at the promyelocyte stage,
or in cell model systems, appearing soon after the induction of
monocytic differentiation. We wished to determine if this
developmentally related interaction is a consequence of myeloid
differentiation or an intrinsic differentiating stimulus. Because the
elevated Myb:Maf status seen in differentiating cells can be
recapitulated by overexpression of c-Maf in myeloid cell lines, we
inducibly expressed the c-Maf cDNA in 2 bipotent human myeloid
progenitor cells. Elevated levels of c-Maf protein led to marked
increases in Myb:Maf complexes and the accumulation of
monocyte/macrophage cells, followed by eventual programmed cell death.
Analysis of targets that could mediate these phenotypic changes
indicated that c-Maf likely plays a key role in myeloid cell
development through dual mechanisms; inhibition of a select set of
c-Myb regulated targets, such as Bcl-2 and CD13/APN,
coupled with the activation of as yet undefined
differentiation-promoting genes.
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