Loss of BAF complexes strengthens CTCF binding and alters genome structure
Researchers disrupted BAF function in mammalian cells to observe how the resulting loss changes chromatin architecture and CTCF occupancy.
Pharmacological inhibition reveals conserved response
Scientists used pharmacological inhibitors and ARID1A deletion to stop BAF complex activity across different tissues. This approach caused increased accessibility at sites where CTCF normally binds. The changes occurred consistently in various mammalian cell types tested during the study.
Antagonistic relationship between complexes confirmed
Genomic profiling showed that removing cBAF led to higher occupancy of CTCF and SMC3 proteins. These results demonstrate an antagonistic relationship between canonical BAF and CTCF, cohesin complexes. The loss of cBAF also restructured the three-dimensional organization of the genome.
Topological domains become smaller
Large topologically associating domains were subdivided into smaller insulated structures after BAF disruption. Long-range enhancer, promoter loops were replaced by shorter loops anchored at CTCF-enriched sites. PBAF was recruited to these new sites of increased CTCF occupancy following depletion.
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