Journal
IMMUNITY
Volume 17, Issue 5, Pages 665-676Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(02)00452-1
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Funding
- NHLBI NIH HHS [HL-07237, HL-36110] Funding Source: Medline
- NIAID NIH HHS [AI-23483, AI-31599] Funding Source: Medline
- NIGMS NIH HHS [GM-07151] Funding Source: Medline
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PU.1 and GATA transcription factors appear to antagonize each other's function in the development of distinct lineages of the hematopoietic system. In contrast, we demonstrate that PU.1, like GATA-2, is essential for the generation of mast cells. PU.1-/- hematopoietic progenitors can be propagated in IL-3 and differentiate into mast cells or macrophages upon restoration of PU.1 activity. Using these progenitors and a conditionally activatable PU.1 protein, we show that PU.1 can negatively regulate expression of the GATA-2 gene. In the absence of GATA-2, PU.1 promotes macrophage but not mast cell differentiation. Reexpression of GATA-2 in such progenitors enables the generation of mast cells. We propose a developmental model in which cooperative function or antagonistic crossregulation by PU.1 of GATA-2 promotes distinct myeloid cell fates.
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