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J Biol Chem, Vol. 274, Issue 3, 1801-1813, January 15, 1999
From the Proliferation, differentiation, and apoptosis are
tightly regulated during hematopoiesis, allowing amplification along
specific lineages while preventing excessive proliferation of immature cells. The MCL1 member of the BCL2 family is
up-regulated during the induction of monocytic differentiation
(~10-fold with 12-O-tetradecanoylphorbol 13-acetate
(TPA)). MCL1 has effects similar to those of
BCL2, up-regulation promoting viability, but differs from
BCL2 in its rapid inducibility and its pattern of
expression. Nuclear factors that regulate MCL1
transcription have now been identified, extending the previous
demonstration of signal transduction through mitogen-activated protein
kinase. A 162-base pair segment of the human MCL1 5'-flank was found to direct luciferase reporter activity, allowing ~10-fold induction with TPA that was suppressible upon inhibition of the extracellular signal-regulated kinase (ERK) pathway. Serum response factor (SRF), Elk-1, and Sp1 bound to cognate sites within this segment, SRF and Elk-1 acting coordinately to affect both basal activity and TPA inducibility, whereas Sp1 affected basal activity only. Thus, the mechanism of the TPA-induced increase in
MCL1 expression seen in myelomonocytic cells at early
stages of differentiation involves signal transduction through ERKs and
transcriptional activation through SRF/Elk-1. This finding provides a
parallel to early response genes (e.g. c-FOS
and EGR1) that affect maturation commitment in these cells
and therefore suggests a means through which enhancement of cell
viability may be linked to the induction of differentiation.
Regulation of MCL1 through a Serum Response
Factor/Elk-1-mediated Mechanism Links Expression of a
Viability-promoting Member of the BCL2 Family to the
Induction of Hematopoietic Cell Differentiation
,,,,
,
Departments of Pharmacology and Toxicology
and the Department of Medicine, Dartmouth Medical School,
Hanover, New Hampshire 03755-3835 and the ** Department of Pathology,
Cancer Biology Laboratories, Cornell University,
Ithaca, New York 14853
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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