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 Blood, 15 June 2007, Vol. 109, No. 12, pp. 5230-5233.
Prepublished online as a Blood First Edition Paper on March 5, 2007; DOI 10.1182/blood-2007-02-072983.

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HEMATOPOIESIS

Brief Report

Friend of GATA-1–independent transcriptional repression: a novel mode of GATA-1 function

Kirby D. Johnson1, Meghan E. Boyer1, Jeong-Ah Kang2, Amittha Wickrema2, Alan B. Cantor3, and Emery H. Bresnick1

1 Department of Pharmacology, University of Wisconsin School of Medicine, Madison; 2 Section of Hematology Oncology, University of Chicago, IL; 3 Division of Pediatric Hematology/Oncology, Children's Hospital Boston, MA

The GATA-1–interacting protein Friend Of GATA-1 (FOG-1) is essential for the proper transcriptional activation and repression of numerous GATA-1 target genes. Although FOG-1–independent activation by GATA-1 has been described, all known examples of GATA-1–mediated repression are FOG-1 dependent. In the GATA-1–null G1E cell line, estrogen receptor ligand binding domain (ER) chimeras of either wild-type GATA-1 or a FOG-1–binding defective mutant of GATA-1 repressed several genes similarly upon activation with ß-estradiol. Repression also occurred in a FOG-1–null cell line expressing ER–GATA-1 and during ex vivo erythropoiesis. At the Lyl1 and Rgs18 loci, we found highly restricted occupancy by GATA-1 and GATA-2, indicating that these genes are direct targets of GATA factor regulation. The identification of genes repressed by GATA-1 independent of FOG-1 defines a novel mode of GATA-1–mediated transcriptional regulation.


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