Leukemogenesis caused by dysfunction of hematopoietic GATA factors

GATA1是红细胞/巨核细胞分化所必需的转录因子。我们发现启动子-近端增强子中的三个元件在体内对Gata1基因的时空表达有不同的贡献。此外，我们发现GATA1-FOG1相互作用的缺失导致独特的膜蛋白组合缺乏，导致溶血。我们还发现GATA1有两个独立的交易激活结构域，N-TAD和C-TAD，它们都保留了体内正常造血的冗余和特定活性。

GATA1 is a transcription factor essential for erythroid/megakaryocytic cell differentiation. We found that three elements within promoter-proximal enhancer differentially contribute to spatio-temporal expression of the Gata1 gene in vivo. In addition, we found that loss of the GATA1-FOG1 interaction causes a unique combination of membrane protein deficiency, leading to the hemolysis. We also found that GATA1 has two independent transactivation domains, N-TAD and C-TAD, and both retain redundant as well as specific activities for proper hematopoiesis in vivo.