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Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892
IFN consensus sequence binding protein (ICSBP; IFN regulatory
factor-8) is a transcription factor of the IFN regulatory factor
family. Disruption of this gene results in a leukemia-like disease in
mice. To investigate the role of ICSBP in myeloid cell development,
lineage marker-negative (Lin-) bone marrow progenitor
cells were purified from ICSBP+/+ and
ICSBP-/- mice and tested for gene expression and
colony-forming ability. ICSBP was expressed in Lin-
progenitor cells, and its levels were markedly increased by IFN-
.
The colony-forming potential of ICSBP-/- progenitor cells
was grossly abnormal, as they gave rise to a disproportionately high
number of granulocyte colonies and many fewer macrophage colonies.
IFN- inhibited colony formation, while promoting macrophage
maturation in ICSBP+/+ cells. In contrast, the effects of
IFN- were completely absent in ICSBP-/- progenitors.
By retrovirus transduction we tested whether reintroduction of ICSBP
restores a normal colony-forming potential in -/- progenitor cells.
The wild-type ICSBP, but not transcriptionally defective mutants,
corrected abnormal colony formation by increasing macrophage colonies
and decreasing granulocyte colonies. Taken together, ICSBP plays a
critical role in myeloid cell development by controlling lineage
selection and is indispensable for IFN--dependent modulation of
progenitor cell maturation.
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