The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers

Burak H. Alver, Kimberly H. Kim, Ping Lu, Xiaofeng Wang, Haley E. Manchester, Weishan Wang, Jeffrey R. Haswell, Peter J. Park () and Charles W. M. Roberts ()
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Burak H. Alver: Harvard Medical School
Kimberly H. Kim: Dana-Farber Cancer Institute
Ping Lu: Dana-Farber Cancer Institute
Xiaofeng Wang: Dana-Farber Cancer Institute
Haley E. Manchester: Dana-Farber Cancer Institute
Weishan Wang: Dana-Farber Cancer Institute
Jeffrey R. Haswell: Dana-Farber Cancer Institute
Peter J. Park: Harvard Medical School
Charles W. M. Roberts: Dana-Farber Cancer Institute

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract Genes encoding subunits of SWI/SNF (BAF) chromatin remodelling complexes are collectively altered in over 20% of human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and cell fate are poorly understood. Utilizing mouse embryonic fibroblast and cancer cell line models, here we show via ChIP-seq and biochemical assays that SWI/SNF complexes are preferentially targeted to distal lineage specific enhancers and interact with p300 to modulate histone H3 lysine 27 acetylation. We identify a greater requirement for SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed regions than in transcribed regions. Our data further demonstrate that SWI/SNF-dependent distal enhancers are essential for controlling expression of genes linked to developmental processes. Our findings thus establish SWI/SNF complexes as regulators of the enhancer landscape and provide insight into the roles of SWI/SNF in cellular fate control.

Date: 2017
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DOI: 10.1038/ncomms14648

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