Tissue-specific CTCF–cohesin-mediated chromatin architecture delimits enhancer 
interactions and function in vivo

Hanssen, L. L. P.; Kassouf, M. T.; Oudelaar, A. M.; Biggs, D.; Preece, C.; Downes, D. J.; Gosden, M.; Sharpe, J. A.; Sloane-Stanley, J. A.; Hughes, J. R.; Davies, B.; Higgs, D. R.

doi:10.1038/ncb3573

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Tissue-specific CTCF–cohesin-mediated chromatin architecture delimits enhancer interactions and function in vivo

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Oudelaar, A. M.
Lise Meitner Group Genome Organization and Regulation, MPI for Biophysical Chemistry, Max Planck Society;

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Citation

Hanssen, L. L. P., Kassouf, M. T., Oudelaar, A. M., Biggs, D., Preece, C., Downes, D. J., et al. (2017). Tissue-specific CTCF–cohesin-mediated chromatin architecture delimits enhancer interactions and function in vivo. Nature Cell Biology, 19(8), 952-961. doi:10.1038/ncb3573.

Cite as: https://hdl.handle.net/21.11116/0000-0007-6179-4

Abstract

The genome is organized via CTCF–cohesin-binding sites, which partition chromosomes into 1–5 megabase (Mb) topologically associated domains (TADs), and further into smaller sub-domains (sub-TADs). Here we examined in vivo an ∼80 kb sub-TAD, containing the mouse α-globin gene cluster, lying within a ∼1 Mb TAD. We find that the sub-TAD is flanked by predominantly convergent CTCF–cohesin sites that are ubiquitously bound by CTCF but only interact during erythropoiesis, defining a self-interacting erythroid compartment. Whereas the α-globin regulatory elements normally act solely on promoters downstream of the enhancers, removal of a conserved upstream CTCF–cohesin boundary extends the sub-TAD to adjacent upstream CTCF–cohesin-binding sites. The α-globin enhancers now interact with the flanking chromatin, upregulating expression of genes within this extended sub-TAD. Rather than acting solely as a barrier to chromatin modification, CTCF–cohesin boundaries in this sub-TAD delimit the region of chromatin to which enhancers have access and within which they interact with receptive promoters.