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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.

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


  • Yu C
  • Cantor AB
  • Yang H
  • Browne C
  • Wells RA
  • Fujiwara Y
  • Orkin SH


The Journal of experimental medicine

Publication Data

June 3, 2002

Associated Grants

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

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