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.
journal_name
Cell Repjournal_title
Cell reportsauthors
Sen P,Luo J,Hada A,Hailu SG,Dechassa ML,Persinger J,Brahma S,Paul S,Ranish J,Bartholomew Bdoi
10.1016/j.celrep.2017.02.017subject
Has Abstractpub_date
2017-02-28 00:00:00pages
2135-2147issue
9issn
2211-1247pii
S2211-1247(17)30182-1journal_volume
18pub_type
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