Coregulator-Dependent Facilitation of Chromatin Occupancy by GATA-1

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 101; no. 4; pp. 980 - 985
• Main Authors: Pal, Saumen, Cantor, Alan B., Johnson, Kirby D., Moran, Tyler B., Boyer, Meghan E., Orkin, Stuart H., Bresnick, Emery H.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 27-01-2004; National Acad Sciences
• Subjects: Acetylation; Biological Sciences; Carrier Proteins - physiology; Cell Line, Transformed; Cell lines; CHO cells; Chromatin; Chromatin - metabolism; Deoxyribonucleic acid; DNA; DNA-Binding Proteins - genetics; DNA-Binding Proteins - physiology; Erythroid-Specific DNA-Binding Factors; FOG-1 protein; GATA transcription factors; GATA-2 protein; GATA2 Transcription Factor; Genetics; Histones; Memory interference; Nuclear Proteins - physiology; Proteins; Repression; Retroviridae; Reverse Transcriptase Polymerase Chain Reaction; Transcription Factors - genetics; Transcription Factors - physiology; Transcription, Genetic
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.0307612100

Coregulator recruitment by DNA-bound factors results in chromatin modification and protein-protein interactions, which regulate transcription. However, the mechanism by which the Friend of GATA (FOG) coregulator mediates GATA factor-dependent transcription is unknown. We showed previously that GATA-1 replaces GATA-2 at an upstream region of the GATA-2 locus, and that this GATA switch represses GATA-2. Genetic complementation analysis in FOG-1-null hematopoietic precursors revealed that FOG-1 is not required for establishment or maintenance of the active GATA-2 domain, but is critical for the GATA switch. Analysis of GATA factor binding to additional loci also revealed FOG-1-dependent GATA switches. Thus, FOG-1 facilitates chromatin occupancy by GATA-1 at sites bound by GATA-2. We propose that FOG-1 is a prototype of a new class of coregulators termed chromatin occupancy facilitators, which confer coregulation in certain contexts via enhancing trans-acting factor binding to chromatin in vivo.