Journal
EMBO JOURNAL
Volume 24, Issue 13, Pages 2367-2378Publisher
WILEY
DOI: 10.1038/sj.emboj.7600703
Keywords
chromatin; FOG-1; GATA-1; gene repression; NuRD
Categories
Funding
- NHLBI NIH HHS [T32-HL07775-10, T32 HL007775, HL01015, T32HL0743926] Funding Source: Medline
- NIDDK NIH HHS [R01 DK058044, DK58044, R37 DK058044] Funding Source: Medline
Ask authors/readers for more resources
Transcription factor GATA-1 and its cofactor FOG-1 coordinate erythroid cell maturation by activating erythroid-specific genes and repressing genes associated with the undifferentiated state. Here we show that FOG-1 binds to the NuRD corepressor complex in vitro and in vivo. The interaction is mediated by a small conserved domain at the extreme N-terminus of FOG-1 that is necessary and sufficient for NuRD binding. This domain defines a novel repression module found in diverse transcriptional repressors. NuRD is present at GATA-1/FOG-1-repressed genes in erythroid cells in vivo. Point mutations near the N-terminus of FOG-1 that abrogate NuRD binding block gene repression by FOG-1. Finally, the ability of GATA-1 to repress transcription was impaired in erythroid cells expressing mutant forms of FOG-1 that are defective for NuRD binding. Together, these studies show that FOG-1 and likely other FOG-like proteins are corepressors that link GATA factors to histone deacetylation and nucleosome remodeling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available