FIG 1.

GATA2 transactivates GATA1 in the HSPCs of MG-G1 mice, and haploid insufficiency of the Gata2 gene rescues MG-G1 mice from perinatal lethality. (A) Structure of MG-G1 BAC DNA. The G1MDR sequence was deleted in the context of Gata1 BAC DNA. The three regulatory elements of the Gata1 gene, shown as black (G1HE), gray (dbG), and white (CACCC) rectangles, were combined to generate MG-G1. IE, erythroid cell-specific 1st exon of the Gata1 gene. (B) Gata1 mRNA levels in LSK cells from E14.5 livers. Note that MG-G1 embryos showed 3.3-fold more Gata1 mRNA but that the increase was abrogated by Gata2 haploid insufficiency. WT, wild type. (C) Pale appearance of an MG-G1 embryo compared to that of a wild-type littermate embryo at E17.5. The anemic appearance was rescued by the reduction of GATA2 abundance. (D) Genotyping results for neonates born from crosses of MG-G1 and wild-type mice (left) or MG-G1 and Gata2^GFP/+ mice (right). The total numbers of neonates examined, the Mendelian expected numbers, and the actual numbers of neonates born alive are shown. (E) Retarded growth of MG-G1 neonates was rescued by Gata2 haploid insufficiency. (F) Kaplan-Meier survival curves for MG-G1 and MG-G1::Gata2^GFP/+ mice after birth. The numbers of mice examined in this cohort were 18 and 13 for MG-G1 and MG-G1::Gata2^GFP/+ mice, respectively. Data shown are the means ± SD for three mice. **, P < 0.01; ***, P < 0.001 (unpaired Student's t test).