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Xist RNA antagonizes the SWI/SNF chromatin remodeler BRG1 on the inactive X chromosome.


ABSTRACT: The noncoding RNA Xist recruits silencing factors to the inactive X chromosome (Xi) and facilitates re-organization of Xi structure. Here, we examine the mouse epigenomic landscape of Xi and assess how Xist alters chromatin accessibility. Xist deletion triggers a gain of accessibility of select chromatin regions that is regulated by BRG1, an ATPase subunit of the SWI/SNF chromatin-remodeling complex. In vitro, RNA binding inhibits nucleosome-remodeling and ATPase activities of BRG1, while in cell culture Xist directly interacts with BRG1 and expels BRG1 from the Xi. Xist ablation leads to a selective return of BRG1 in cis, starting from pre-existing BRG1 sites that are free of Xist. BRG1 re-association correlates with cohesin binding and restoration of topologically associated domains (TADs) and results in the formation of de novo Xi 'superloops'. Thus, Xist binding inhibits BRG1's nucleosome-remodeling activity and results in expulsion of the SWI/SNF complex from the Xi.

SUBMITTER: Jegu T 

PROVIDER: S-EPMC6421574 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Xist RNA antagonizes the SWI/SNF chromatin remodeler BRG1 on the inactive X chromosome.

Jégu Teddy T   Blum Roy R   Cochrane Jesse C JC   Yang Lin L   Wang Chen-Yu CY   Gilles Maud-Emmanuelle ME   Colognori David D   Szanto Attila A   Marr Sharon K SK   Kingston Robert E RE   Lee Jeannie T JT  

Nature structural & molecular biology 20190121 2


The noncoding RNA Xist recruits silencing factors to the inactive X chromosome (Xi) and facilitates re-organization of Xi structure. Here, we examine the mouse epigenomic landscape of Xi and assess how Xist alters chromatin accessibility. Xist deletion triggers a gain of accessibility of select chromatin regions that is regulated by BRG1, an ATPase subunit of the SWI/SNF chromatin-remodeling complex. In vitro, RNA binding inhibits nucleosome-remodeling and ATPase activities of BRG1, while in cel  ...[more]

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