Gene Regulation

How chromatin remodeling complexes find their genomic targets and how their assembly is regulated.

The SWI/SNF chromatin remodeling complex is an enzyme that slides and evicts nucleosomes to open chromatin for other factors, so that changes in gene expression follow changes in accessibility. We’re interested in finding how this complex transcription while accessibility stays the same. The complex therefore also acts as a scaffold, recruiting regulatory proteins independently of its remodeling activity. We study what controls that scaffolding and how the partners SWI/SNF recruits produce specific changes in gene expression.

Our current projects focus on two ways SWI/SNF partners are regulated. One is post-translational modification of SWI/SNF subunits. CARM1 methylates an arginine on the core subunit BAF155. This methylation does not change which version of the complex assembles, but it changes the proteins the complex contacts, particularly the RNA processing machinery, and can alter transcription without any change in chromatin accessibility. The other input is RNA itself. SWI/SNF and related remodelers bind RNA and act at several steps of the transcription cycle, including polymerase pausing, splicing, and 3′ end processing, and RNA can tune the complex’s interactions on a transcript-by-transcript basis.

Our goal is to define how SWI/SNF and related remodelers select their regulatory partners and how that selection shapes gene regulation beyond accessibility. We use chromatin profiling, gene expression analysis, and interaction proteomics to link specific modifications and RNA contacts to the genes they control.

Key Publications

  • Sokolowski M, Scoville D, Kuhlers PC, Raab J. Arginine methylation of BAF155 regulates interactions with RNA processing machinery. bioRxiv (2026). 10.64898/2026.05.18.726059
  • Raab JR, Smith KN, Spear CC, Manner CJ, Calabrese JM, Magnuson T. SWI/SNF remains localized to chromatin in the presence of SCHLAP1. Nature Genetics (2019). 10.1038/s41588-018-0272-z
  • Zhao S, et al. TNRC18 engages H3K9me3 to mediate silencing of endogenous retrotransposons. Nature (2023). 10.1038/s41586-023-06688-z
  • Raab JR, Resnick S, Magnuson T. Genome-wide transcriptional regulation mediated by biochemically distinct SWI/SNF complexes. PLoS Genetics (2015). 10.1371/journal.pgen.1005748