GoKawiilStudy finds SWI/SNF chromatin remodelers help position CTCF and cohesin in 3D genome folding
Researchers at Weill Cornell Medicine used mouse models with mutations in SWI/SNF complex genes Arid1a and Pbrm1, alongside a Ctcf-deficient strain, to study how these remodeling proteins influence chromatin's three-dimensional architecture. The team combined ATAC-seq and RNA-seq data across multiple biological replicates to examine how SWI/SNF activity relates to the positioning of CTCF and cohesin, two proteins known to organize genome loops and domains.
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SWI/SNF complex genes like ARID1A and PBRM1 are frequently mutated in human cancers, so clarifying their role in genome architecture could help explain how such mutations drive disease, according to the study's experimental design. The findings may eventually inform research into how disruptions in chromatin folding contribute to abnormal gene expression in tumors, though the excerpt provided does not detail specific results.
- Mouse models with Arid1a, Pbrm1 and Ctcf mutations were used to probe chromatin architecture.
- ATAC-seq and RNA-seq with multiple replicates per condition formed the core experimental approach.
- SWI/SNF genes studied are also known cancer-associated genes, linking chromatin structure research to tumor biology.
Source: nature.com — Debek, 2026-10-28
Published there as: “SWI/SNF complexes shape 3D chromatin architecture through CTCF and cohesin”
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