Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription

Summary: The ARID1A subunit of SWI/SNF chromatin remodeling complexes is a potent tumor suppressor. Here, a degron is applied to detect rapid loss of chromatin accessibility at thousands of loci where ARID1A acts to generate accessible minidomains of nucleosomes. Loss of ARID1A also results in the r...

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Autores principales:	Seraina Blümli, Nicola Wiechens, Meng-Ying Wu, Vijender Singh, Marek Gierlinski, Gabriele Schweikert, Nick Gilbert, Catherine Naughton, Ramasubramanian Sundaramoorthy, Joby Varghese, Robert Gourlay, Renata Soares, David Clark, Tom Owen-Hughes
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	ARID1A SWI/SNF EP300 BAF chromatin remodeling nucleosomes Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/04921146582c4b71a0ec2443dd1ee13e
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spelling	oai:doaj.org-article:04921146582c4b71a0ec2443dd1ee13e2021-11-04T04:29:37ZAcute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription2211-124710.1016/j.celrep.2021.109943https://doaj.org/article/04921146582c4b71a0ec2443dd1ee13e2021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2211124721014169https://doaj.org/toc/2211-1247Summary: The ARID1A subunit of SWI/SNF chromatin remodeling complexes is a potent tumor suppressor. Here, a degron is applied to detect rapid loss of chromatin accessibility at thousands of loci where ARID1A acts to generate accessible minidomains of nucleosomes. Loss of ARID1A also results in the redistribution of the coactivator EP300. Co-incident EP300 dissociation and lost chromatin accessibility at enhancer elements are highly enriched adjacent to rapidly downregulated genes. In contrast, sites of gained EP300 occupancy are linked to genes that are transcriptionally upregulated. These chromatin changes are associated with a small number of genes that are differentially expressed in the first hours following loss of ARID1A. Indirect or adaptive changes dominate the transcriptome following growth for days after loss of ARID1A and result in strong engagement with cancer pathways. The identification of this hierarchy suggests sites for intervention in ARID1A-driven diseases.Seraina BlümliNicola WiechensMeng-Ying WuVijender SinghMarek GierlinskiGabriele SchweikertNick GilbertCatherine NaughtonRamasubramanian SundaramoorthyJoby VargheseRobert GourlayRenata SoaresDavid ClarkTom Owen-HughesElsevierarticleARID1ASWI/SNFEP300BAFchromatin remodelingnucleosomesBiology (General)QH301-705.5ENCell Reports, Vol 37, Iss 5, Pp 109943- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	ARID1A SWI/SNF EP300 BAF chromatin remodeling nucleosomes Biology (General) QH301-705.5
spellingShingle	ARID1A SWI/SNF EP300 BAF chromatin remodeling nucleosomes Biology (General) QH301-705.5 Seraina Blümli Nicola Wiechens Meng-Ying Wu Vijender Singh Marek Gierlinski Gabriele Schweikert Nick Gilbert Catherine Naughton Ramasubramanian Sundaramoorthy Joby Varghese Robert Gourlay Renata Soares David Clark Tom Owen-Hughes Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription
description	Summary: The ARID1A subunit of SWI/SNF chromatin remodeling complexes is a potent tumor suppressor. Here, a degron is applied to detect rapid loss of chromatin accessibility at thousands of loci where ARID1A acts to generate accessible minidomains of nucleosomes. Loss of ARID1A also results in the redistribution of the coactivator EP300. Co-incident EP300 dissociation and lost chromatin accessibility at enhancer elements are highly enriched adjacent to rapidly downregulated genes. In contrast, sites of gained EP300 occupancy are linked to genes that are transcriptionally upregulated. These chromatin changes are associated with a small number of genes that are differentially expressed in the first hours following loss of ARID1A. Indirect or adaptive changes dominate the transcriptome following growth for days after loss of ARID1A and result in strong engagement with cancer pathways. The identification of this hierarchy suggests sites for intervention in ARID1A-driven diseases.
format	article
author	Seraina Blümli Nicola Wiechens Meng-Ying Wu Vijender Singh Marek Gierlinski Gabriele Schweikert Nick Gilbert Catherine Naughton Ramasubramanian Sundaramoorthy Joby Varghese Robert Gourlay Renata Soares David Clark Tom Owen-Hughes
author_facet	Seraina Blümli Nicola Wiechens Meng-Ying Wu Vijender Singh Marek Gierlinski Gabriele Schweikert Nick Gilbert Catherine Naughton Ramasubramanian Sundaramoorthy Joby Varghese Robert Gourlay Renata Soares David Clark Tom Owen-Hughes
author_sort	Seraina Blümli
title	Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription
title_short	Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription
title_full	Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription
title_fullStr	Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription
title_full_unstemmed	Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription
title_sort	acute depletion of the arid1a subunit of swi/snf complexes reveals distinct pathways for activation and repression of transcription
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/04921146582c4b71a0ec2443dd1ee13e
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Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription

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