Analysis of Genetically Diverse Macrophages Reveals Local and Domain-wide Mechanisms that Control Transcription Factor Binding and Function
Open accessAbstract
Non-coding genetic variation is a major driver of phenotypic diversity and allows the investigation of mechanisms that control gene expression. Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages. We observed substantial differences associated with distinct molecular pathways. Evaluating genetic variation provided evidence for roles of ∼100 TFs in shaping lineage-determining factor binding. Unexpectedly, a substantial fraction of strain-specific factor binding could not be explained by local mutations. Integration of genomic features with chromatin interaction data provided evidence for hundreds of connected cis-regulatory domains associated with differences in transcription factor binding and gene expression. This system and the >250 datasets establish a substantial new resource for investigation of how genetic variation affects cellular phenotypes.
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The Il1b distal region was among the genomic regions most enriched for p65/RELA binding in BMDMs.
“The Il1b distal region was among the most enriched genomic regions in p65/RELA binding (Fig. 4J and Extended Data Fig. 6B).”
From Chromatin remodelling drives immune cell–fibroblast communication in heart failure (2024) · cites this paper as [29]
The Results section on TF binding reports P65 ChIP-seq in BMDMs, but does not identify the Il1b distal region or rank its P65 binding against other genomic regions. Searches for Il1b, interleukin-1 beta, and the claimed enrichment found no passage addressing that comparison; page numbers were unavailable in our copy. (LLM, conf=0.74)
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MMARGE: Motif Mutation Analysis for Regulatory Genomic Elements
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Self-citationA Chinese hamster transcription start site atlas that enables targeted editing of CHO cells
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Self-citationHi-C as a molecular rangefinder to examine genomic rearrangements
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- Authors
- Link, V. M., Duttke, S. H., Chun, H. B., Holtman, I. R., Westin, E., Hoeksema, M. A., Abe, Y., Skola, D., Romanoski, C. E., Tao, J., Fonseca, G. J., Troutman, T. D., Spann, N. J., Strid, T., Sakai, M., Yu, M., Hu, R., Fang, R., Metzler, D., Ren, B., & Glass, C. K.
- Affiliations
- University of California San Diego (US)
- University Medical Center Groningen (NL)
- University of Arizona (US)
- Ludwig Cancer Research (US)
- Ludwig-Maximilians-Universität München (DE)
- Ludwig Cancer Research (BE)
- Corresponding author
- Glass, Christopher K.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 173
- Issue
- 7
- Pages
- 1796-1809.e17
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC6003872
- OpenAlex
- W2803237856
- Cited by
- 182
- References
- 67
- Citations by year
- 2026: 9 · 2025: 19 · 2024: 23 · 2023: 19 · 2022: 23 · 2021: 34 · 2020: 30 · 2019: 19 · 2018: 6
- FWCI
- 7.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, other-oa)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- eScholarship (California Digital Library) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Funders
- NIH (DK091183, CA17390, GM085764, DK063491, T32DK007541, T32DK007044, T32CA009523)
- Leducq Transatlantic Network
- CRI-Irvington
- German Research Council
- Collaborative Research Center 1243 (project A16)
- Swedish Society for Medical Research
- Sarnoff Cardiovascular Research Foundation
- Dutch MS Research Foundation
- Gemmy and Mibeth Tichelaar Foundation
- NIH-NHLBI (R00123485)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- macrophages, genetic variation, transcription factor binding, nascent transcription, transcription start sites, mouse strains, chromatin interactions, gene expression regulation, macrophage activation
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Binding Sites, Bone Marrow Cells, Enhancer Elements, Genetic, Female, Gene Expression Regulation, Lipopolysaccharides, Macrophages, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins, Transcription Factors, Genetic Variation, Trans-Activators, Cluster Analysis, Mice, Inbred NOD, CCAAT-Enhancer-Binding Protein-beta, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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