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Induction of hematopoietic commitment and erythromyeloid differentiation in
embryonal stem cells constitutively expressing c-myb
P Melotti and B Calabretta
Departments of Microbiology and Immunology, Jefferson Cancer Institute,
Thomas Jefferson University, Philadelphia, PA USA.
To provide insight into the mechanisms by which c-myb regulates
hematopoiesis, we analyzed the expression of markers for multiple
hematopoietic lineages in differentiating parental embryonic stem (ES)
cells and in ES cells transfected with c-myb or with a mutant c-myb
deficient in DNA binding and assessed the ability of these cells to undergo
hematopoietic commitment and colony formation. Undifferentiated ES cells
transfected with intact c-myb, but not cells transfected with mutant c-myb,
expressed CD34, c-kit, GATA1, and flt3 mRNA as well as surface CD34, c-kit,
and flt3 product. In contrast, the kinetics of GATA-2 mRNA expression was
identical in parental and Myb-transfected ES cells. Transient expression
assays suggested transactivation of gene expression dependent on
interaction with Myb binding sites in the CD34 and GATA1 5' flanking
regions. Undifferentiated parental and c-myb mutant-transfected ES cells
were not clonogenic, whereas c-myb transfectants formed erythromyeloid
colonies in methylcellulose cultures in the absence of added hematopoietic
growth factors and, at higher frequency, in the presence of kit and flt-3
ligands. Colony formation was suppressed by treatment with antisense
oligodeoxynucleotides specifically downregulating c-kit and flt-3
expression. These findings indicate that c-myb regulates hematopoietic
commitment and progenitor cell proliferation and differentiation through
the activation of certain genes that define the stem/progenitor cell
compartment.
Volume 87,
Issue 6,
pp. 2221-2234,
03/15/1996
Copyright © 1996 by The American Society of Hematology
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