Migliaccio Anna Rita, Rana Rosa Alba, Sanchez Massimo, Lorenzini Rodolfo, Centurione Lucia, Bianchi Lucia, Vannucchi Alessandro Maria, Migliaccio Giovanni, Orkin Stuart H
Department of Biomorphology, University G. D'Annunzio, 66100 Chieti, Italy.
J Exp Med. 2003 Feb 3;197(3):281-96. doi: 10.1084/jem.20021149.
Here it is shown that the phenotype of adult mice lacking the first enhancer (DNA hypersensitive site I) and the distal promoter of the GATA-1 gene (neo Delta HS or GATA-1(low) mutants) reveals defects in mast cell development. These include the presence of morphologically abnormal alcian blue(+) mast cells and apoptotic metachromatic(-) mast cell precursors in connective tissues and peritoneal lavage and numerous (60-70% of all the progenitors) "unique" trilineage cells committed to erythroid, megakaryocytic, and mast pathways in the bone marrow and spleen. These abnormalities, which were mirrored by impaired mast differentiation in vitro, were reversed by retroviral-mediated expression of GATA-1 cDNA. These data indicate an essential role for GATA-1 in mast cell differentiation.
本文表明，缺乏GATA-1基因的第一个增强子（DNA高敏位点I）和远端启动子的成年小鼠（neo Delta HS或GATA-1(low)突变体）的表型显示出肥大细胞发育缺陷。这些缺陷包括结缔组织和腹腔灌洗中存在形态异常的阿尔辛蓝阳性肥大细胞和凋亡的异染性阴性肥大细胞前体，以及骨髓和脾脏中大量（占所有祖细胞的60-70%）致力于红细胞、巨核细胞和肥大细胞途径的“独特”三系细胞。这些异常在体外肥大细胞分化受损中得到反映，并通过逆转录病毒介导的GATA-1 cDNA表达得以逆转。这些数据表明GATA-1在肥大细胞分化中起重要作用。
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