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Vol. 13, No. 20, pp. 2691-2703, October 15, 1999
1 Laboratory of Molecular Genetics of Hemopoietic Stem
Cells, Clinical Research Institute of Montréal, Montréal,
Québec H2W 1R7, Canada; 2 Department of Medicine and
3 Division of Hematology Maisonneuve-Rosemont Hospital,
Université de Montréal, Montréal, Québec H3C
3J7, Canada; 4 Department of Molecular and Human Genetics and
Program in Developmental Biology, Baylor College of Medicine, Houston,
Texas 77030 USA; 5 Division of Molecular Carcinogenesis, The
Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands;
6 Department of Genetics, Case Western Reserve University,
Cleveland, Ohio 44106 USA
The murine Polycomb-Group (PcG) proteins Eed and Bmi1 govern
axial patterning during embryonic development by segment-specific repression of Hox gene expression. The two proteins engage in distinct multimeric complexes that are thought to use a common molecular mechanism to render the regulatory regions of Hox and other downstream target genes inaccessible to transcriptional activators. Beyond axial patterning, Bmi1 is also involved in hemopoiesis because a loss-of-function allele causes a profound decrease in bone marrow progenitor cells. Here, evidence is presented that is consistent with an antagonistic function of eed and
Bmi1 in hemopoietic cell proliferation. Heterozygosity for an
eed null allele causes marked myelo- and lymphoproliferative
defects, indicating that eed is involved in the negative
regulation of the pool size of lymphoid and myeloid progenitor cells.
This antiproliferative function of eed does not appear to be
mediated by Hox genes or the tumor suppressor locus
p16INK4a/p19ARF because
expression of these genes was not altered in eed mutants. Intercross experiments between eed and Bmi1 mutant mice
revealed that Bmi1 is epistatic to eed in the control
of primitive bone marrow cell proliferation. However, the genetic
interaction between the two genes is cell-type specific as the presence
of one or two mutant alleles of eed trans-complements the
Bmi1-deficiency in pre-B bone marrow cells. These studies thus
suggest that hemopoietic cell proliferation is regulated by the
relative contribution of repressive (Eed-containing) and enhancing
(Bmi1-containing) PcG gene complexes.
[Key Words: eed; Bmi1; Polycomb-Group (PcG) genes; hemopoiesis; cellular proliferation]
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