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I am looking for examples (if any) of genomic regions which regulates the activity of enhancers, either augmenting or reducing it. Essentially some kind of enhancers (or repressors) of enhancers to make a Russian doll analogy. I know about epigenetic markings but I am really looking at an example of a DNA region directly acting on a enhancer similar to an enhancer acting directly onto a promoter.

I am asking that because I couldn't find any examples and was wondering if I missed such a report/paper.

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    $\begingroup$ Do you care if it's from a viral genome? $\endgroup$ – Atl LED Mar 13 '15 at 14:14
  • $\begingroup$ @AtlLED If it is a DNA virus then that works. I am interested in DNA secondary and tertiary structures. $\endgroup$ – cagliari2005 Mar 13 '15 at 15:38
  • $\begingroup$ It could be possible that certain enhancer regions can bind the regulatory proteins with higher affinity than other enhancer regions, thus surpressing the amount of activation of the genes regulated by the 'lower affinity enhancer region'. $\endgroup$ – Wolgast Mar 30 '15 at 12:21
  • $\begingroup$ @Wolgast Interesting idea. This would be some kind of gene regulation via competition. I don't know if this actually happens in the cell (i.e. if some TF are in concentration ranges which would provoke such effect) but in any case it is worth looking into this. Thanks. $\endgroup$ – cagliari2005 Mar 30 '15 at 15:33
  • $\begingroup$ Yes indeed. I'm am interested where this will lead you. Let me know if you find anything! :-) $\endgroup$ – Wolgast Mar 30 '15 at 17:39
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If you're looking for a strictly and directly DNA-DNA mediated effect (no histones, no transcription involved) I'd look for sequence effects on chromatin remodelling, modulating access of transcription factors (TFs) to their elements. Something about this might be in this paper: Szerlong, H. J., & Hansen, J. C. (2011). Nucleosome distribution and linker DNA: connecting nuclear function to dynamic chromatin structure. Biochemistry and Cell Biology = Biochimie et Biologie Cellulaire, 89(1), 24–34. doi:10.1139/O10-139

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