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Journal Article

Long non-coding RNAs direct the SWI/SNF complex to cell type-specific enhancers

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Müller-McNicoll,  Michaela       
Cardio-Pulmonary Institute (CPI), Goethe University Frankfurt, Frankfurt, Germany;
Goethe University Frankfurt, Institute for Molecular Biosciences, Frankfurt, Germany;
Max Planck Fellow Group RNA regulation Group, Prof. Michaela Müller-McNicoll, Max Planck Institute of Biophysics, Max Planck Society;

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Citation

Oo, J. A., Warwick, T., Pálfi, K., Lam, F., McNicoll, F., Prieto-Garcia, C., et al. (2025). Long non-coding RNAs direct the SWI/SNF complex to cell type-specific enhancers. Nature Communications, 16: 131. doi:10.1038/s41467-024-55539-6.


Cite as: https://hdl.handle.net/21.11116/0000-0010-5F92-F
Abstract
The coordination of chromatin remodeling is essential for DNA accessibility and gene expression control. The highly conserved and ubiquitously expressed SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex plays a central role in cell type- and context-dependent gene expression. Despite the absence of a defined DNA recognition motif, SWI/SNF binds lineage specific enhancers genome-wide where it actively maintains open chromatin state. It does so while retaining the ability to respond dynamically to cellular signals. However, the mechanisms that guide SWI/SNF to specific genomic targets have remained elusive. Here we demonstrate that trans-acting long non-coding RNAs (lncRNAs) direct the SWI/SNF complex to cell type-specific enhancers. SWI/SNF preferentially binds lncRNAs and these predominantly bind DNA targets in trans. Together they localize to enhancers, many of which are cell type-specific. Knockdown of SWI/SNF- and enhancer-bound lncRNAs causes the genome-wide redistribution of SWI/SNF away from enhancers and a concomitant differential expression of spatially connected target genes. These lncRNA-SWI/SNF-enhancer networks support an enhancer hub model of SWI/SNF genomic targeting. Our findings reveal that lncRNAs competitively recruit SWI/SNF, providing a specific and dynamic layer of control over chromatin accessibility, and reinforcing their role in mediating enhancer activity and gene expression.