Figure 7. An Artificially Recruited Secondary Transcription Factor Drives Transcription in the Absence of p65.

On the left is a cartoon illustrating our model for the events occurring at Trap-80–independent promoters. In wild-type cells, initial p65 binding brings about an undefined change to target promoters, which allows the binding of various secondary transcription factors. Once bound, these can drive the recruitment of pol-II, and so enable transcription. In p65-knockout cells, secondary transcription factors cannot bind and no transcription takes place. If binding of a secondary transcription factor is artificially restored (in this case Sp1), transcription is rescued at promoters that can recruit the relevant co-factors (in this case TAF_II250).

On the right, p65-knockout cells were transduced with a retrovirus expressing a fusion of the p65 DBD with the Sp1 TAD (red triangles, p65DBD-Sp1), and expression of Mip-2 and Ip-10 mRNA was compared to untransduced wild-type and p65-knockout fibroblasts. The result is representative of three experiments.