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Blood, 15 April 2001, Vol. 97, No. 8, pp. 2300-2307
HEMATOPOIESIS
Lineage switch induced by overexpression of Ets family
transcription factor PU.1 in murine erythroleukemia cells
Toshiyuki Yamada,
Masaaki Abe,
Toshinori Higashi,
Hitomi Yamamoto,
Fumiko Kihara-Negishi,
Takuya Sakurai,
Toshikazu Shirai, and
Tsuneyuki Oikawa
From the Department of Cell Genetics, Sasaki Institute,
and the Department of Pathology, Juntendo University School of
Medicine, Tokyo, Japan.
PU.1 is an Ets family transcription factor essential for
myelomonocyte and B-cell development. We previously showed that
overexpression of PU.1 in murine erythroleukemia (MEL) cells inhibits
growth and erythroid differentiation and induces apoptosis of the
cells. In an effort to identify target genes of PU.1 concerning these phenomena by using a messenger RNA differential display strategy, we
found that some myeloid-specific and lymphoid-specific genes, such as
the osteopontin gene, are transcriptionally up-regulated in MEL cells
after overexpression of PU.1. We then found that expression of several
myelomonocyte-specific genes, including the CAAT-enhancer-binding
protein- and granulocyte-macrophage colony-stimulating factor
receptor genes, was induced in MEL cells after overexpression of
PU.1. B-cell-specific genes were also examined, and expression
of the CD19 gene was found to be induced. Expression of the
myelomonocyte-specific proteins CD11b and F4/80 antigen but not the
B-cell-specific proteins B220 and CD19 was also induced. After
overexpression of PU.1, MEL cells became adherent and phagocytic and
showed enhanced nitroblue tetrazolium reduction activity. Expression of
myelomonocyte-specific and B-cell-specific genes was not induced when
a mutant PU.1 with part of the activation domain deleted (a change
found to inhibit erythroid differentiation of MEL cells) was expressed.
These results indicate that PU.1 induces a lineage switch in MEL cells
toward myelomonocytic cells and that its activation domain is essential
for this effect. The results also suggest that the pathway of the
lineage switch is distinct from that of inhibition of erythroid
differentiation in MEL cells.
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