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Growth Disturbance in Fetal Liver Hematopoiesis of Mll-Mutant Mice
Hideshi Yagi,
Kenji Deguchi,
Atsufumi Aono,
Yoshihiko Tani,
Tadamitsu Kishimoto, and
Toshihisa Komori
From the Department of Medicine III, Osaka University Medical School,
Osaka, Japan.
The MLL (ALL-1, HRX) gene is frequently involved in chromosomal
translocations in acute leukemia and has homology with Drosophila trithorax, which controls homeobox gene expression and
embryogenesis. To elucidate the function of Mll, we generated mice with
a mutated Mll locus. Mice with a homozygous mutation were embryonic
lethal and died at embryonic day 11.5 to 14.5, showing edematous bodies and petechiae. Histological examination revealed that hematopoietic cells were decreased in the liver of homozygous embryos, although they
were composed of erythroid, myeloid, monocytic, and megakaryocytic cells with normal differentiation. Colony-forming assays using cells
from fetal livers and yolk sacs showed that the number of colonies was
markedly reduced and many of the colonies delayed to be recognized in
Mllmu/mu embryos, although some of the colonies from
Mllmu/mu embryos developed similarly with that from
Mll+/+ and Mll+/mu embryos, suggesting
the delayed onset of the proliferation of hematopoitic precursors.
These data show that the hematopoietic precursors were greatly reduced
in mutant mice, and suggest that Mll functions as a regulator of the
growth of hematopoietic precursors.
Blood, Vol. 92 No. 1 (July 1), 1998:
pp. 108-117
© 1998 by The American Society of Hematology.
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