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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

The Journal of Experimental MedicinePublished 3 June 2002Open access
Channing Yu, Alan Cantor, Haidi Yang, Carol Browne, Richard A. Wells, Yuko Fujiwara
Citations598
SJR quartileQ1
SJR score5.83
SNIP1.99
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TL;DR

Findings suggest that GATA-1 is required for specification of this lineage during hematopoietic development, and mice lacking the ability to produce eosinophils should prove useful in ascertaining the role of eosInophils in a variety of inflammatory or allergic disorders.

Abstract

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.

Keywords

Medicine