ArticleNature communications2022
A leukemia-protective germline variant mediates chromatin module formation via transcription factor nucleation.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Enhancer-mediated Etv4 activation stimulates osteogenic differentiation.Nature communications · 2026Article
- Generative AI creates synthetic regulatory DNA sequences for precision gene control.Nature genetics · 2026Article
- Designing synthetic regulatory elements using the generative AI framework DNA-Diffusion.Nature genetics · 2026Article
- FAIR sharing of Chromatin Tracing datasets using the newly developed 4DN FISH Omics Format.ArXiv · 2025Article
- Context transcription factors establish cooperative environments and mediate enhancer communication.Nature genetics · 2024Article
- Non-coding variants impact cis-regulatory coordination in a cell type-specific manner.Genome biology · 2024Article
- Image-based 3D genomics through chromatin tracing.Nature reviews. Methods primers · 2024Article
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Authors and funding
21 authors at 7 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-coding variants coordinate transcription factor (TF) binding and chromatin mark enrichment changes over regions spanning >100 kb. These molecularly coordinated regions are named "variable chromatin modules" (VCMs), providing a conceptual framework of how regulatory variation might shape complex traits. To better understand the molecular mechanisms underlying VCM formation, here, we mechanistically dissect a VCM-modulating noncoding variant that is associated with reduced chronic lymphocytic leukemia (CLL) predisposition and disease progression. This common, germline variant constitutes a 5-bp indel that controls the activity of an AXIN2 gene-linked VCM by creating a MEF2 binding site, which, upon binding, activates a super-enhancer-like regulatory element. This triggers a large change in TF binding activity and chromatin state at an enhancer cluster spanning >150 kb, coinciding with subtle, long-range chromatin compaction and robust AXIN2 up-regulation. Our results support a model in which the indel acts as an AXIN2 VCM-activating TF nucleation event, which modulates CLL pathology.
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