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.
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3 June 2002
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June 03 2002
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,
Channing Yu
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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Alan B. Cantor,
Alan B. Cantor
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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Haidi Yang,
Haidi Yang
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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Carol Browne,
Carol Browne
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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Richard A. Wells,
Richard A. Wells
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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Yuko Fujiwara,
Yuko Fujiwara
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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Stuart H. Orkin
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
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Channing Yu
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
Alan B. Cantor
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
Haidi Yang
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
Carol Browne
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
Richard A. Wells
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
Yuko Fujiwara
Department of Pediatric Oncology, Dana Farber Cancer Institute and Children's Hospital, Harvard Medical School and the Howard Hughes Medical Institute, Boston, MA 02115
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: [email protected]
H. Yang's current address is Novartis Pharmaceutical Corp., 556 Morris Ave., Summit, NJ 07901-1398.
R. Wells' current address is Ontario Cancer Institute, University of Toronto, 610 University Ave., Toronto, Ontario, Canada M5G 2M9.
Received:
April 23 2002
Accepted:
May 02 2002
Online ISSN: 1540-9538
Print ISSN: 0022-1007
The Rockefeller University Press
2002
J Exp Med (2002) 195 (11): 1387–1395.
Article history
Received:
April 23 2002
Accepted:
May 02 2002
Citation
Channing Yu, Alan B. Cantor, Haidi Yang, Carol Browne, Richard A. Wells, Yuko Fujiwara, Stuart H. Orkin; Targeted Deletion of a High-Affinity GATA-binding Site in the GATA-1 Promoter Leads to Selective Loss of the Eosinophil Lineage In Vivo . J Exp Med 3 June 2002; 195 (11): 1387–1395. doi: https://doi.org/10.1084/jem.20020656
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