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      Reconstruction of enhancer–target networks in 935 samples of human primary cells, tissues and cell lines

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          Abstract

          Kevin Yip and colleagues report a method for determining the target genes of enhancers in specific cells and tissues by combining global trends across many samples with sample-specific information, and considering the joint effect of multiple enhancers. They apply their method to reconstruct enhancer–target networks in 935 samples of human primary cells, tissues and cell lines.

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          Most cited references17

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          Chromosome Conformation Capture Carbon Copy (5C): a massively parallel solution for mapping interactions between genomic elements.

          Physical interactions between genetic elements located throughout the genome play important roles in gene regulation and can be identified with the Chromosome Conformation Capture (3C) methodology. 3C converts physical chromatin interactions into specific ligation products, which are quantified individually by PCR. Here we present a high-throughput 3C approach, 3C-Carbon Copy (5C), that employs microarrays or quantitative DNA sequencing using 454-technology as detection methods. We applied 5C to analyze a 400-kb region containing the human beta-globin locus and a 100-kb conserved gene desert region. We validated 5C by detection of several previously identified looping interactions in the beta-globin locus. We also identified a new looping interaction in K562 cells between the beta-globin Locus Control Region and the gamma-beta-globin intergenic region. Interestingly, this region has been implicated in the control of developmental globin gene switching. 5C should be widely applicable for large-scale mapping of cis- and trans- interaction networks of genomic elements and for the study of higher-order chromosome structure.
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            Genomic Views of Distant-Acting Enhancers

            Preface In contrast to changes in protein-coding sequences, the significance of noncoding DNA variation in human disease has been minimally explored. A recent torrent of genome-wide association studies suggests that noncoding variation represents a significant risk factor for common disorders, but the mechanisms by which they contribute to disease remain largely obscure. Distant-acting transcriptional enhancers - a major category of functional noncoding DNA - are likely involved in many developmental and disease-relevant processes. Genome-wide approaches for their discovery and functional characterization are now available and provide a growing knowledgebase for the systematic exploration of their role in human biology and disease susceptibility.
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              Genome architectures revealed by tethered chromosome conformation capture and population-based modeling.

              We describe tethered conformation capture (TCC), a method for genome-wide mapping of chromatin interactions. By performing ligations on solid substrates rather than in solution, TCC substantially enhances the signal-to-noise ratio, thereby facilitating a detailed analysis of interactions within and between chromosomes. We identified a group of regions in each chromosome in human cells that account for the majority of interchromosomal interactions. These regions are marked by high transcriptional activity, suggesting that their interactions are mediated by transcriptional machinery. Each of these regions interacts with numerous other such regions throughout the genome in an indiscriminate fashion, partly driven by the accessibility of the partners. As a different combination of interactions is likely present in different cells, we developed a computational method to translate the TCC data into physical chromatin contacts in a population of three-dimensional genome structures. Statistical analysis of the resulting population demonstrates that the indiscriminate properties of interchromosomal interactions are consistent with the well-known architectural features of the human genome.
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                Author and article information

                Journal
                Nature Genetics
                Nat Genet
                Springer Nature
                1061-4036
                1546-1718
                September 4 2017
                September 4 2017
                :
                :
                Article
                10.1038/ng.3950
                28869592
                f3c72dd0-d402-40a7-8b2f-42b1f82dfc6f
                © 2017
                History

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