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Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 2849-2858
Commitment to the Monocytic Lineage Occurs in the Absence of the
Transcription Factor PU.1
Gregory W. Henkel,
Scott R. McKercher,
Pieter J.M. Leenen, and
Richard A. Maki
From The Burnham Institute, La Jolla, CA, and Department of
Immunology, Erasmus University, Rotterdam, Netherlands.
Mice homozygous for the disruption of the PU.1 (Spi-1) gene do not
produce mature macrophages. In determining the role of PU.1 in
macrophage differentiation, the present study investigated whether or
not there was commitment to the monocytic lineage in the absence of
PU.1. Early PU.1 / myeloid colonies were generated from neonate
liver under conditions that promote primarily macrophage and
granulocyte/macrophage colonies. These PU.1/ colonies were found
to contain cells with monocytic characteristics as determined by
nonspecific esterase stain and the use of monoclonal antibodies that
recognize early monocyte precursors, including Moma-2, ER-MP12, ER-MP20, and ER-MP58. In addition, early myeloid cells could be grown
from PU.1/ fetal liver cultures in the presence of
granulocyte-macrophage colony-stimulating factor (GM-CSF). Similar to
the PU.1 null colonies, the GM-CSF-dependent cells also possessed
early monocytic characteristics, including the ability to phagocytize
latex beads. The ability of PU.1/ progenitors to commit to the
monocytic lineage was also verified in vivo by flow cytometry and
cytochemical analysis of primary neonate liver cells. The combined data
shows that PU.1 is absolutely required for macrophage development after
commitment to this lineage.
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