Extended Data Fig. 6: MCC of CTCF sites at loci that are active in erythroid or ES cells shows that highly punctate interactions occur between CTCF sites and that these correlate with the activity of the intervening chromatin.

Note that contacts from CTCF sites do not correlate strongly with DNase I hypersensitivity. a, Capture from the CTCF site downstream of the enhancers at the β-globin locus. This site interacts strongly and precisely with the CTCF site upstream of the genes. These sites are in a convergent orientation. These interactions are not present in ES cells when the gene is inactive despite there being similar levels of CTCF occupancy at these sites in both tissues. b, Capture at an intergenic CTCF site at the Cd47 locus in erythroid cells shows strong tissue-specific interactions between convergent sites upstream that are not present in ES cells when the gene is inactive. c, At the Slc25a37 locus (which encodes mitoferrin), the CTCF site downstream of the enhancers interacts strongly with the convergent CTCF site at the promoter of the gene in a tissue-specific manner. d, Strong and highly punctate contacts are seen between multiple CTCF sites at the gene-dense Klf1 locus. e, At the Myc locus, highly specific, punctate contacts occur between the CTCF sites on either side of the gene and its regulatory elements. These contacts correlate with transcription (the gene is transcribed more in ES cells than erythroid cells). f, Similarly, at the Sox2 locus, highly specific long-range contacts occur between CTCF sites and these are highly tissue-specific (they are absent in erythroid cells in which the gene is inactive). DNase-seq (green) and ChIP–seq of CTCF and RAD21 are shown for both erythroid cells and ES cells. The RAD21 and CTCF ChIP–seq are normalized using a spike-in of human cells.