ArticleNature communications2018
Exploiting genetic variation to uncover rules of transcription factor binding and chromatin accessibility.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
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- Multiplex base editing of BCL11A regulatory elements to treat sickle cell disease.Cell reports. Medicine · 2025Article
- Integrating genetic variation with deep learning provides context for variants impacting transcription factor binding during embryogenesis.Genome research · 2025Article
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- Individual-specific functional epigenomics reveals genetic determinants of adverse metabolic effects of glucocorticoids.Cell metabolism · 2021Article
- Cell-type-specific effects of genetic variation on chromatin accessibility during human neuronal differentiation.Nature neuroscience · 2021Article
- Mechanisms underlying divergent responses of genetically distinct macrophages to IL-4.Science advances · 2021Article
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- Distinct properties and functions of CTCF revealed by a rapidly inducible degron system.Cell reports · 2021Article
- ATACdb: a comprehensive human chromatin accessibility database.Nucleic acids research · 2021Article
- Rare genetic variation at transcription factor binding sites modulates local DNA methylation profiles.PLoS genetics · 2020Article
- Unravelling the complex genetics of common kidney diseases: from variants to mechanisms.Nature reviews. Nephrology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Single-nucleotide variants that underlie phenotypic variation can affect chromatin occupancy of transcription factors (TFs). To delineate determinants of in vivo TF binding and chromatin accessibility, we introduce an approach that compares ChIP-seq and DNase-seq data sets from genetically divergent murine erythroid cell lines. The impact of discriminatory single-nucleotide variants on TF ChIP signal enables definition at single base resolution of in vivo binding characteristics of nuclear factors GATA1, TAL1, and CTCF. We further develop a facile complementary approach to more deeply test the requirements of critical nucleotide positions for TF binding by combining CRISPR-Cas9-mediated mutagenesis with ChIP and targeted deep sequencing. Finally, we extend our analytical pipeline to identify nearby contextual DNA elements that modulate chromatin binding by these three TFs, and to define sequences that impact kb-scale chromatin accessibility. Combined, our approaches reveal insights into the genetic basis of TF occupancy and their interplay with chromatin features.
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