Abstract
The SWI/SNF chromatin remodeling complex is highly conserved from yeast to human, and aberrant SWI/SNF complexes contribute to human disease. The Snf5/SMARCB1/INI1 subunit of SWI/SNF is a tumor suppressor frequently lost in pediatric rhabdoid cancers. We examined the effects of Snf5 loss on the composition, nucleosome binding, recruitment, and remodeling activities of yeast SWI/SNF. The Snf5 subunit is shown by crosslinking-mass spectrometry (CX-MS) and subunit deletion analysis to interact with the ATPase domain of Snf2 and to form a submodule consisting of Snf5, Swp82, and Taf14. Snf5 promotes binding of the Snf2 ATPase domain to nucleosomal DNA and enhances the catalytic and nucleosome remodeling activities of SWI/SNF. Snf5 is also required for SWI/SNF recruitment by acidic transcription factors. RNA-seq analysis suggests that both the recruitment and remodeling functions of Snf5 are required in vivo for SWI/SNF regulation of gene expression. Thus, loss of SNF5 alters the structure and function of SWI/SNF.
Original language | English (US) |
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Pages (from-to) | 2135-2147 |
Number of pages | 13 |
Journal | Cell Reports |
Volume | 18 |
Issue number | 9 |
DOIs | |
State | Published - Feb 28 2017 |
Keywords
- BAF47
- Chromatin remodeling
- INI1
- SMARCB1
- SWI/SNF
- Snf5
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology