FOG-1 recruits the NuRD repressor complex to mediate transcriptional repression by GATA-1.
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.[1]References
- FOG-1 recruits the NuRD repressor complex to mediate transcriptional repression by GATA-1. Hong, W., Nakazawa, M., Chen, Y.Y., Kori, R., Vakoc, C.R., Rakowski, C., Blobel, G.A. EMBO J. (2005) [Pubmed]
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