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Blood, Vol. 94 No. 7 (October 1), 1999:
pp. 2310-2318
PU.1 and the Granulocyte- and Macrophage Colony-Stimulating Factor
Receptors Play Distinct Roles in Late-Stage Myeloid Cell
Differentiation
Karen L. Anderson,
Kent A. Smith,
Hugh Perkin,
Gary Hermanson,
Carol-Gay Anderson,
Douglas J. Jolly,
Richard A. Maki, and
Bruce E. Torbett
From The Burnham Institute, La Jolla, CA; the Department of
Immunology, The Scripps Research Institute, La Jolla, CA; Vical, Inc,
San Diego,CA; and Chiron Technologies Center for Gene Therapy, San
Diego, CA.
PU.1 is a hematopoietic cell-specific ets family transcription
factor. Gene disruption of PU.1 results in a cell autonomous defect in
hematopoietic progenitor cells that manifests as abnormal myeloid and
B-lymphoid development. Of the myeloid lineages, no mature macrophages
develop, and the neutrophils that develop are aberrantly and
incompletely matured. One of the documented abnormalities of PU.1 null
(deficient) hematopoietic cells is a failure to express receptors for
granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage (GM)-CSF, and M-CSF. To elucidate the roles of the myeloid growth factor receptors in myeloid cell differentiation, and to distinguish their role from that of PU.1, we have restored expression of the G- and
M-CSF receptors in PU.1-deficient cells using retroviral vectors. We
have similarly expressed PU.1 in these cells. Whereas expression of
growth factor receptors merely allows a PU.1-deficient cell line to
survive and grow in the relevant growth factor, expression of PU.1
enables the development of F4/80+,
Mac-1+/CD11b+ macrophages, expression of
gp91phox and generation of superoxide, and
expression of secondary granule genes for neutrophil collagenase and
gelatinase. These studies reinforce the idea that availability of PU.1
is crucial for normal myeloid development and clarify some of the
molecular events in developing neutrophils and macrophages that are
critically dependent on PU.1.
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