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Blood, Vol. 92 No. 9 (November 1), 1998:
pp. 3226-3239
Mcl-1 in Transgenic Mice Promotes Survival in a Spectrum of
Hematopoietic Cell Types and Immortalization in the Myeloid Lineage
Ping Zhou,
Liping Qian,
Christine K. Bieszczad,
Randolph Noelle,
Michael Binder,
Norman B. Levy, and
Ruth W. Craig
From the Departments of Pharmacology and Toxicology, Pathology,
Anatomy, and Immunology, Dartmouth Medical School, Hanover, NH.
Mcl-1 is a member of the Bcl-2 family that is expressed in early
monocyte differentiation and that can promote viability on transfection
into immature myeloid cells. However, the effects of Mcl-1 are
generally short lived compared with those of Bcl-2 and are not obvious
in some transfectants. To further explore the effects of this gene,
mice were produced that expressed Mcl-1 as a transgene in
hematolymphoid tissues. The Mcl-1 transgene was found to cause moderate
viability enhancement in a wide range of hematopoietic cell types,
including lymphoid (B and T) as well as myeloid cells at both immature
and mature stages of differentiation. However, enhanced hematopoietic
capacity in transgenic bone marrow and spleen was not reflected in any
change in pool sizes in the peripheral blood. In addition, among
transgenic cells, mature T cells remained long lived compared with B
cells and macrophages could live longer than either of these.
Interestingly, when hematopoietic cells were maintained in tissue
culture in the presence of interleukin-3, Mcl-1 enhanced the
probability of outgrowth of continuously proliferating myeloid cell
lines. Thus, Mcl-1 transgenic cells remained subject to normal in vivo
homeostatic mechanisms controlling viable cell number, but these
constraints could be overridden under specific conditions in vitro.
Within the organism, Bcl-2 family members may act at "viability
gates" along the differentiation continuum, functioning as part of a
system for controlled hematopoietic cell amplification. Enforced
expression of even a moderate viability-promoting member of this family
such as Mcl-1, within a conducive intra- and extracellular environment
in isolation from normal homeostatic constraints, can substantially
increase the probability of cell immortalization.
© 1998 by The American Society of Hematology.
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