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Blood, Vol. 94 No. 12 (December 15), 1999:
pp. 4255-4262
c-myb Transactivates the Human Cyclin A1 Promoter and Induces Cyclin
A1 Gene Expression
Carsten Müller,
Rong Yang,
Gregory Idos,
Nicola Tidow,
Sven Diederichs,
Olaf M. Koch,
Walter Verbeek,
Timothy P. Bender, and
H.
Phillip Koeffler
From the Division of Hematology/Oncology, Cedars-Sinai Research
Institute/UCLA School of Medicine, Los Angeles, CA; the Department of
Microbiology, University of Virginia, Charlottesville, VA; and the
Department of Hematology/Oncology, University of Muenster, Muenster,
Germany.
Cyclin A1 differs from other cyclins in its highly restricted
expression pattern. Besides its expression during spermatogenesis, cyclin A1 is also expressed in hematopoietic progenitor cells and in
acute myeloid leukemia. We investigated mechanisms that might
contribute to cyclin A1 expression in hematopoietic cells. Comparison
of cyclin A1 and cyclin A promoter activity in adherent and myeloid
leukemia cell lines showed that the cyclin A1 promoter is
preferentially active in myeloid cell lines. This preferential activity
was present in a small, 335-bp cyclin A1 promoter fragment that
contained several potential c-myb binding sites. Coexpression of a
c-myb expression vector with the cyclin A1 promoter constructs significantly increased the reporter activity in adherent CV-1 as well
as in myeloid U937 cells. Gel-shift assays demonstrated that c-myb
could bind to the cyclin A1 promoter at a binding site located near the
transcription start site. Site-directed mutagenesis of this site
decreased promoter transactivation by 50% in both KCL22 cells that
express high levels of c-myb and in CV-1 cells that were transfected
with c-myb. In addition, transfection of primary human embryonic
fibroblasts with a c-myb expression vector led to induction of the
endogenous cyclin A1 gene. Taken together, c-myb can directly
transactivate the promoter of cyclin A1, and c-myb might be involved in
the high-level expression of cyclin A1 observed in acute myeloid
leukemia. These findings suggest that c-myb induces
hematopoiesis-specific mechanisms of cell cycle regulation.
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