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The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation

ABSTRACT: The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation

PROVIDER: PRJNA635143 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11851566.fastq.gz	Fastqsanger.gz
	SRR11851567.fastq.gz	Fastqsanger.gz
	SRR11851568.fastq.gz	Fastqsanger.gz
	SRR11851569.fastq.gz	Fastqsanger.gz
	SRR11851570.fastq.gz	Fastqsanger.gz

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The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation

Project description:We performed RNA-seq analysis for C2C12 myoblasts as a function of differentiation. Cells were treated with either DMSO or family VIII bromodomain-specific inhibitor PFI-3 at a concentration of 50uM. We find that PFI-3 treatment affects proper differentiation of myoblasts as compared to DMSO-treated C2C12 cells. We conclude that function of mammalian SWI/SNF bromodomains is important for regulation of myoblast differentiation.

2021-07-05 | GSE151218 | GEO

The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation.

Project description:Skeletal muscle regeneration is mediated by myoblasts that undergo epigenomic changes to establish the gene expression program of differentiated myofibers. mSWI/SNF chromatin remodeling enzymes coordinate with lineage-determining transcription factors to establish the epigenome of differentiated myofibers. Bromodomains bind to acetylated lysines on histone N-terminal tails and other proteins. The mutually exclusive ATPases of mSWI/SNF complexes, BRG1 and BRM, contain bromodomains with undefined functional importance in skeletal muscle differentiation. Pharmacological inhibition of mSWI/SNF bromodomain function using the small molecule PFI-3 reduced differentiation in cell culture and in vivo through decreased myogenic gene expression, while increasing cell cycle-related gene expression and the number of cells remaining in the cell cycle. Comparative gene expression analysis with data from myoblasts depleted of BRG1 or BRM showed that bromodomain function was required for a subset of BRG1- and BRM-dependent gene expression. Reduced binding of BRG1 and BRM after PFI-3 treatment showed that the bromodomain is required for stable chromatin binding at target gene promoters to alter gene expression. Our findings demonstrate that mSWI/SNF ATPase bromodomains permit stable binding of the mSWI/SNF ATPases to promoters required for cell cycle exit and establishment of muscle-specific gene expression.

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Genome-wide profiling of SWI/SNF chromatin remodeler BRAHMA (BRM) and BRM Interacting Protein 1/2 (BRIP1/2) in Arabidopsis

Project description:SWI/SNF chromatin remodeling complexes control gene expression by regulating chromatin structure. However, the full subunit composition of SWI/SNF complexes in plants remains unclear. Here we show that BRAHMA Interacting Protein 1 (BRIP1) and BRIP2 in Arabidopsis thaliana are core subunits of plant SWI/SNF complexes. BRIP1 and 2 are two homolog proteins. brip1 brip2 double mutants exhibit developmental phenotypes and a transcriptome strikingly similar to those of BRAHMA (BRM) mutants. Genetic interaction tests indicated that BRIP1 and 2 act together with BRM to regulate gene expression. Furthermore, BRIP1 and 2 physically interact with BRM-containing SWI/SNF complexes, and extensively co-localize with BRM at endogenous genes. Loss-of-brip1brip2 results in decreased BRM occupancy at almost all BRM target genes and substantially reduced subunits incorporation into the BRM-containing SWI/SNF complexes. Together, our work identifies new core subunits of BRM-containing SWI/SNF complexes in plants, and uncovers the essential role of these subunits in regulating the integrity (assembly) of SWI/SNF complexes in plants.

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Project description:Acquired resistance to tyrosine kinase inhibitors (TKI), such as osimertinib used to treat EGFR-mutant lung adenocarcinomas, limits long-term efficacy and is frequently caused by non-genetic mechanisms. Here, we define the chromatin accessibility and gene regulatory signatures of osimertinib sensitive and resistant EGFR-mutant cell and patient-derived models and uncover a role for mammalian SWI/SNF chromatin remodeling complexes in TKI resistance. By profiling mSWI/SNF genome-wide localization, we identify both shared and cancer cell line-specific gene targets underlying the resistant state. Importantly, genetic and pharmacologic disruption of the SMARCA4/SMARCA2 mSWI/SNF ATPases re-sensitizes a subset of resistant models to osimertinib via inhibition of mSWI/SNF-mediated regulation of cellular programs governing cell proliferation, epithelial-to-mesenchymal transition, epithelial cell differentiation, and NRF2 signaling. These data highlight the role of mSWI/SNF complexes in supporting TKI resistance and suggest potential utility of mSWI/SNF inhibitors in TKI-resistant lung cancers.

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