Targeted Deletion of a High-Affinity GATA-binding Site in the GATA-1 Promoter Leads to Selective Loss of the Eosinophil Lineage In Vivo
Copyright policy )Targeted Deletion of a High-Affinity GATA-binding Site in the GATA-1 Promoter Leads to Selective Loss of the Eosinophil Lineage In Vivo
Transcription factor GATA-1 reprograms immature myeloid cells to three different hematopoietic lineages-erythroid cells, megakaryocytes, and eosinophils. GATA-1 is essential for maturation of erythroid and megakaryocytic precursors, as revealed by gene targeting in mice. Here we demonstrate that deletion of a high-affinity GATA-binding site in the GATA-1 promoter, an element presumed to mediate positive autoregulation of GATA-1 expression, leads to selective loss of the eosinophil lineage. These findings suggest that GATA-1 is required for specification of this lineage during hematopoietic development. Mice lacking the ability to produce eosinophils should prove useful in ascertaining the role of eosinophils in a variety of inflammatory or allergic disorders.
- Dana-Farber Cancer Institute United States
- Harvard University United States
- Children's Hospital Tunisia
- Howard Hughes Medical Institute United States
Male, Base Sequence, Molecular Sequence Data, Cell Differentiation, Mice, Transgenic, Article, DNA-Binding Proteins, Eosinophils, Mice, Gene Expression Regulation, Mutagenesis, Site-Directed, Animals, Erythroid-Specific DNA-Binding Factors, Cell Lineage, Erythropoiesis, GATA1 Transcription Factor, Leukopoiesis, Mast Cells, RNA, Messenger, Interleukin-5, Promoter Regions, Genetic
Male, Base Sequence, Molecular Sequence Data, Cell Differentiation, Mice, Transgenic, Article, DNA-Binding Proteins, Eosinophils, Mice, Gene Expression Regulation, Mutagenesis, Site-Directed, Animals, Erythroid-Specific DNA-Binding Factors, Cell Lineage, Erythropoiesis, GATA1 Transcription Factor, Leukopoiesis, Mast Cells, RNA, Messenger, Interleukin-5, Promoter Regions, Genetic
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