Figure 5.

Combinatorial model of adult β-globin gene repression. (A) Wild-type β-globin gene showing known transcription factor DNA-binding sites. (B) Model shows interaction between these DNA binding sites with HMG1+2, BP1 and BP2 factors. Collectively, they provide DNA–protein and protein–protein interactions needed to form a stable silencing complex. (C) Modification of the model in which disruption of the stable DNA–protein, protein–protein silencing complex (seen here by in vitro mutagenesis of functional assays by the DNA mutation of BP1 binding) activates the β-globin gene in K562 environment. (D) Silencing disruption in erythroid cells via βLCR interaction with the β-promoter, leading to gene activation.