Targeted Deletion of a High-Affinity GATA-binding Site in the GATA-1 Promoter Leads to Selective Loss of the Eosinophil Lineage In Vivo

By Channing Yu, A. Cantor, Haidi Yang, C. Browne, R. Wells, Y. Fujiwara, Stuart H. Orkin. Journal of Experimental Medicine, 2002

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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.

Subfields: Epidemiology, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/670ea2113b0d4893d816e4fc411cdc696212e774

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