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loops, cell, chromatin, loop, contact, data, article, gene, types, hic, google, scholar, type, expression, propensity, cas, supplementary, ipsc, fig, htals, ipsccm, differences, hkac, anchors, genome, imbalance, differential, called, identified, found, ipscs, frequency, nature, haplotypes, individuals, set, reads, ipsccms, figure, samples, significant, regulatory, genes, showing, union, looping, shown, haplotype, ctals, allelic,

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source data file writing—review & editing nature portfolio omics research privacy policy modulating wnt/beta-catenin signaling advertising supplementary data 3 supplementary data 4–14 supplementary data 15 source social media nature communications supplementary figure 1c highly chimeric nature open chromatin architecture supplementary figure 1h supplementary figure 6g supplementary figure 2g reprints supplementary figure 1a atac-seq data generation supplementary figure 3a largely open question supplementary figure 3b chip-seq data generation supplementary figure 1b supplementary figure 5a supplementary figure 5b supplementary figure 5c supplementary figure 6a supplementary figure 6c supplementary figure 6d supplementary figure 6e supplementary figure 6f mouse neural development supplementary figure 3c supplementary figure 6b rna-seq data generated crispr-mediated chromosomal looping processed data files data statistically limited long-range interacting elements cohesin-mediated chromatin loops supplementary figure 2 supplementary figure 4 supplementary figure 7 supplementary figure 5 open chromatin paired-end data

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         headline:Subtle changes in chromatin loop contact propensity are associated with differential gene regulation and expression
         description:While genetic variation at chromatin loops is relevant for human disease, the relationships between contact propensity (the probability that loci at loops physically interact), genetics, and gene regulation are unclear. We quantitatively interrogate these relationships by comparing Hi-C and molecular phenotype data across cell types and haplotypes. While chromatin loops consistently form across different cell types, they have subtle quantitative differences in contact frequency that are associated with larger changes in gene expression and H3K27ac. For the vast majority of loci with quantitative differences in contact frequency across haplotypes, the changes in magnitude are smaller than those across cell types; however, the proportional relationships between contact propensity, gene expression, and H3K27ac are consistent. These findings suggest that subtle changes in contact propensity have a biologically meaningful role in gene regulation and could be a mechanism by which regulatory genetic variants in loop anchors mediate effects on expression. It is currently unclear how quantitative changes in chromatin loop propensity contribute to differential gene regulation. Here, the authors use phased Hi-C, RNA-seq, and ChIP-seq to show that subtle changes in loop propensity associate with differential gene regulation across cell types and haplotypes.
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      headline:Subtle changes in chromatin loop contact propensity are associated with differential gene regulation and expression
      description:While genetic variation at chromatin loops is relevant for human disease, the relationships between contact propensity (the probability that loci at loops physically interact), genetics, and gene regulation are unclear. We quantitatively interrogate these relationships by comparing Hi-C and molecular phenotype data across cell types and haplotypes. While chromatin loops consistently form across different cell types, they have subtle quantitative differences in contact frequency that are associated with larger changes in gene expression and H3K27ac. For the vast majority of loci with quantitative differences in contact frequency across haplotypes, the changes in magnitude are smaller than those across cell types; however, the proportional relationships between contact propensity, gene expression, and H3K27ac are consistent. These findings suggest that subtle changes in contact propensity have a biologically meaningful role in gene regulation and could be a mechanism by which regulatory genetic variants in loop anchors mediate effects on expression. It is currently unclear how quantitative changes in chromatin loop propensity contribute to differential gene regulation. Here, the authors use phased Hi-C, RNA-seq, and ChIP-seq to show that subtle changes in loop propensity associate with differential gene regulation across cell types and haplotypes.
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