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Targeted deletion of a high-affinity GATA-binding site in the GATA-1 promoter leads to selective loss of the eosinophil lineage in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12045237

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.

Pubmed ID: 12045237 RIS Download

Mesh terms: Animals | Base Sequence | Cell Differentiation | Cell Lineage | DNA-Binding Proteins | Eosinophils | Erythroid-Specific DNA-Binding Factors | Erythropoiesis | GATA1 Transcription Factor | Gene Expression Regulation | Interleukin-5 | Leukopoiesis | Male | Mast Cells | Mice | Mice, Transgenic | Molecular Sequence Data | Mutagenesis, Site-Directed | Promoter Regions, Genetic | RNA, Messenger | Response Elements | Sequence Deletion | Transcription Factors

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Associated grants

  • Agency: NCI NIH HHS, Id: CA-82175-03

Mouse Genome Informatics (Data, Gene Annotation)

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