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Blood, Vol. 96 No. 3 (August 1), 2000:
pp. 910-916
GATA factor transgenes under GATA-1 locus control rescue
germline GATA-1 mutant deficiencies
Satoru Takahashi,
Ritsuko Shimizu,
Naruyoshi Suwabe,
Takashi Kuroha,
Keigyou Yoh,
Jun Ohta,
Shigeko Nishimura,
Kim-Chew Lim,
James Douglas Engel, and
Masayuki Yamamoto
From the Institute of Basic Medical Sciences and Center for
Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba,
Japan; and Department of Biochemistry, Molecular Biology and Cell
Biology, Northwestern University, Evanston, IL.
GATA-1 germline mutation in mice results in embryonic
lethality due to defective erythroid cell maturation, and thus other hematopoietic GATA factors do not compensate for the loss of
GATA-1. To determine whether the obligate presence of
GATA-1 in erythroid cells is due to its distinct
biochemical properties or spatiotemporal patterning, we attempted to
rescue GATA-1 mutant mice with hematopoietic GATA factor complementary
DNAs (cDNAs) placed under the transcriptional control of the GATA-1
gene. We found that transgenic expression of a GATA-1 cDNA fully
abrogated the GATA-1-deficient phenotype. Surprisingly, GATA-2 and
GATA-3 factors expressed from the same regulatory cassette also rescued
the embryonic lethal phenotype of the GATA-1 mutation. However,
adult mice rescued with the latter transgenes developed anemia, while
GATA-1 transgenic mice did not. These results demonstrate that the
transcriptional control dictating proper GATA-1 accumulation is the
most critical determinant of GATA-1 activity during erythropoiesis. The
results also show that there are biochemical distinctions among the
hematopoietic GATA proteins and that during adult hematopoiesis the
hematopoietic GATA factors are not functionally equivalent.
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