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

• Published in: Blood Vol. 109; no. 12; pp. 5230 - 5233
• Main Authors: Johnson, Kirby D., Boyer, Meghan E., Kang, Jeong-Ah, Wickrema, Amittha, Cantor, Alan B., Bresnick, Emery H.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 15-06-2007; The Americain Society of Hematology; American Society of Hematology
• Series: Hematopoiesis
• Subjects: Animals; Binding Sites; Biological and medical sciences; GATA1 Transcription Factor - genetics; GATA1 Transcription Factor - physiology; Gene Expression Regulation; Hematologic and hematopoietic diseases; Hematopoiesis; Medical sciences; Mice; Mutation; Nuclear Proteins - genetics; Receptors, Estrogen - genetics; Recombinant Fusion Proteins; Transcription Factors - genetics; Transcription, Genetic; Signal transduction; Transcription repressor; Hematology; Transcription factor GATA1
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood-2007-02-072983

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 β-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.