| First Author | Hanssen LLP | Year | 2017 |
| Journal | Nat Cell Biol | Volume | 19 |
| Issue | 8 | Pages | 952-961 |
| PubMed ID | 28737770 | Mgi Jnum | J:246278 |
| Mgi Id | MGI:5921930 | Doi | 10.1038/ncb3573 |
| Citation | Hanssen LLP, et al. (2017) Tissue-specific CTCF-cohesin-mediated chromatin architecture delimits enhancer interactions and function in vivo. Nat Cell Biol 19(8):952-961 |
| abstractText | 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 approximately 80 kb sub-TAD, containing the mouse alpha-globin gene cluster, lying within a approximately 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 alpha-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 alpha-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. |
