GATA-1 as a regulator of mast cell differentiation revealed by the phenotype of the GATA-1low mouse mutant

被引:185
作者
Migliaccio, AR
Rana, RA
Sanchez, M
Lorenzini, R
Centurione, L
Bianchi, L
Vannucchi, AM
Migliaccio, G
Orkin, SH
机构
[1] Ist Super Sanita, Lab Clin Biochem, I-00161 Rome, Italy
[2] Ist Super Sanita, Cell Biol Lab, I-00161 Rome, Italy
[3] Ist Super Sanita, Lab Serv Qual Sicurezza Anim, I-00161 Rome, Italy
[4] Howard Hughes Med Inst, Boston, MA 02115 USA
[5] Harvard Univ, Sch Med, Dana Farber Canc Inst, Childrens Hosp,Dept Pediat Oncol, Boston, MA 02115 USA
[6] Univ Florence, Dept Hematol, I-50139 Florence, Italy
[7] Univ G DAnnunzio, Dept Biomorphol, I-66100 Chieti, Italy
关键词
mast cells; GATA-1; differentiation; commitment; progenitor cells;
D O I
10.1084/jem.20021149
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 (neoDeltaHS 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.
引用
收藏
页码:281 / 296
页数:16
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