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Blood, Vol. 93 No. 1 (January 1), 1999:
pp. 87-95
Definitive But Not Primitive Hematopoiesis Is Impaired in
jumonji Mutant Mice
Kenji Kitajima,
Mizuyo Kojima,
Kuniko Nakajima,
Shunzo Kondo,
Takahiko Hara,
Atsushi Miyajima, and
Takashi Takeuchi
From the Mitsubishi Kasei Institute of Life Sciences, Institute of
Molecular and Cellular Biosciences, The University of Tokyo, Tokyo,
Japan.
A novel gene, jumonji was identified by a mouse gene trap
strategy. The jumonji gene encodes a protein containing a
putative DNA binding domain. The mice homozygous for jumonji
gene with a BALB/cA genetic background show hypoplasia of the fetal
liver and embryonic lethality, suggesting impaired hematopoiesis. In the peripheral blood of jumonji mutant embryos, the number of fetal liver-derived definitive erythrocytes, but not yolk sac-derived primitive erythrocytes, showed a marked reduction, suggesting that
jumonji mutants die of anemia. The defects of definitive erythrocytes in jumonji mutants seemed to be caused by a
decrease in the numbers of multiple hematopoietic progenitors including colony-forming unit-spleen (CFU-S) in the fetal liver. However, hematopoietic stem cells (HSCs) in the fetal liver of jumonji mutants could reconstitute the hematopoietic system of lethally irradiated recipients. In the fetal liver, the jumonji gene is expressed in fibroblastic cells and endothelial cells, but not in
Lin /c-Kit+/Sca-1+ cells
known to include HSCs. These results suggest that an environmental defect induce the impaired hematopoiesis in the fetal liver of jumonji mutant embryos.
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