Our current model proposes that Bptf-containing complexes like NURF are recruited to the promoter of Smad regulated genes through direct interactions with the Smad transcription factors. To test this model, we initiated chromatin immuno-precipitation (ChIP) experiments to detect the Snf2l component of the NURF complex at Lefty1. As anticipated, we observed significant enrichment of Snf2l at the Neural Plate Specific Enhancer (NPE), a region which contains putative FAST and Smad transcription actor binding sites, of the Lefty1 promoter [58]. This enrichment was dependent on activin-A stimulation and on the presence of Bptf (Figure 5D). Snf2l enrichment correlates with the presence of the activating histone modification H3K4me3 at the 5′ UTR of Lefty1 (Figure 5D). These results are consistent with Bptf recruitment to the promoter of Lefty1 through the Smad transcription factors.
