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Role of GATA-1 in Proliferation and Differentiation of Definitive
Erythroid and Megakaryocytic Cells In Vivo
Satoru Takahashi,
Takuya Komeno,
Naruyoshi Suwabe,
Keigyo Yoh,
Osamu Nakajima,
Sigeko Nishimura,
Takashi Kuroha,
Toshiro Nagasawa, and
Masayuki Yamamoto
From the Institute of Basic Medical Sciences and Center for TARA and
the Division of Hematology, Institute of Clinical Medicine, University
of Tsukuba, Tsukuba, Japan
To elucidate the contributions of GATA-1 to definitive hematopoiesis
in vivo, we have examined adult mice that were rendered genetically
defective in GATA-1 synthesis (Takahashi et al, J Biol Chem
272:12611, 1997). Because the GATA-1 gene is located on the X
chromosome, which is randomly inactivated in every cell, heterozygous
females can bear either an active wild-type or mutant (referred to as
GATA-1.05) GATA-1 allele, consequently leading to variable
anemic severity. These heterozygous mutant mice usually developed
normally, but they began to die after 5 months. These affected animals
displayed marked splenomegaly, anemia, and thrombocytopenia. Proerythroblasts and megakaryocytes massively accumulated in the spleens of the heterozygotes, and we showed that the neomycin resistance gene (which is the positive selection marker in ES cells)
was expressed profusely in the abnormally abundant cells generated in
the GATA-1.05 mutant females. We also observed hematopoiesis outside of the bone marrow in the affected mutant mice. These data
suggest that a small number of GATA-1.05 mutant hematopoietic progenitor cells begin to proliferate vigorously during early adulthood, but because the cells are unable to terminally
differentiate, this leads to progenitor proliferation in the spleen and
consequently death. Thus, GATA-1 plays important in vivo roles for
directing definitive hematopoietic progenitors to differentiate along
both the erythroid and megakaryocytic pathways. The GATA-1 heterozygous mutant mouse shows a phenotype that is analogous to human
myelodysplastic syndrome and thus may serve as a useful model for this
disorder.
Blood, Vol. 92 No. 2 (July 15), 1998:
pp. 434-442
© 1998 by the American Society of Hematology.
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