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Myeloid Development Is Selectively Disrupted in PU.1 Null Mice
Karen L. Anderson,
Kent A. Smith,
Kris Conners,
Scott R. McKercher,
Richard A. Maki, and
Bruce E. Torbett
From The Burnham Institute, La Jolla, CA; and the Department of
Immunology, The Scripps Research Institute, La Jolla, CA.
The ets family transcription factor PU.1 is expressed in
monocytes/macrophages, neutrophils, mast cells, B cells, and early erythroblasts, but not in T cells. We have recently shown that PU.1
gene disruption results in mice with no detectable
monocytes/macrophages and B cells but T-cell development is retained.
Although neutrophil development occurred in these mice, it was delayed
and markedly reduced. We now proceed to demonstrate that PU.1 null
hematopoietic cells fail to proliferate or form colonies in response to
macrophage colony-stimulating factor (M-CSF), granulocyte CSF (G-CSF),
and granulocyte/macrophage CSF (GM-CSF). In contrast, PU.1 null cells did proliferate and form colonies in response to interleukin-3 (IL-3),
although the response was reduced as compared with control littermates.
Compared with control cells, PU.1 null cells had minimal expression of
G- and GM-CSF receptors and no detectable M-CSF receptors. The size of
individual myeloid colonies produced from PU.1 null primitive and
committed myeloid progenitors in the presence of IL-3, IL-6, and stem
cell factor (SCF) were reduced compared with controls. Under these
conditions, PU.1 null progenitors produced neutrophils but not
monocytes/macrophages. These observations suggest that PU.1 gene
disruption induces additional cell-autonomous effects that are
independent of the alterations in myeloid growth factor receptor
expression. Our results demonstrate that PU.1 gene disruption affects a
number of developmentally regulated hematopoietic processes that can,
at least in part, explain the changes in myeloid development and
reduction in myeloid and neutrophil expansion observed in PU.1 null
mice.
Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3702-3710
© 1998 by The American Society of Hematology.
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