The Journal of Experimental Medicine
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Published 3 June 2002. doi:10.1084/jem.20020656
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© Rockefeller University Press, 0022-1007/2002/6/1387/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 11, June 3, 2002 1387-1395

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

Channing Yu, Alan B. Cantor, Haidi Yang, Carol Browne, Richard A. Wells, Yuko Fujiwara and Stuart H. Orkin

Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115

Address correspondence to Stuart H. Orkin, Division of Hematology/Oncology, Children's Hospital, 300 Longwood Ave., Boston, MA 02115. Phone: 617-355-7910; Fax: 617-632-4367; E-mail: stuart_orkin{at}dfci.harvard.edu

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.

Key Words: eosinophil • GATA-1 • gene targeting • hematopoiesis • transcription


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