GATA factor transgenes under GATA-1 locus control rescue germline GATA-1 mutant deficiencies.

摘要: GATA-1 germline mutation in mice results 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 obligate presence cells is its distinct biochemical properties or spatiotemporal patterning, we attempted rescue mutant with factor complementary DNAs (cDNAs) placed under transcriptional control gene. We found that transgenic expression a cDNA fully abrogated GATA-1–deficient phenotype. Surprisingly, GATA-2 GATA-3 expressed from same regulatory cassette also rescued lethal phenotype mutation. However, adult latter transgenes developed anemia, while did not. These demonstrate dictating proper accumulation most critical determinant activity during erythropoiesis. The show there are distinctions among proteins hematopoiesis functionally equivalent.