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Co-regulation of transcription by BRG1 and Brm, two mutually exclusive SWI/SNF ATPase subunits

ABSTRACT: Co-regulation of transcription by BRG1 and Brm, two mutually exclusive SWI/SNF ATPase subunits

PROVIDER: PRJNA398033 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5928800.fastq.gz	Fastqsanger.gz
	SRR5928810.fastq.gz	Fastqsanger.gz
	SRR5928820.fastq.gz	Fastqsanger.gz
	SRR5928801.fastq.gz	Fastqsanger.gz
	SRR5928811.fastq.gz	Fastqsanger.gz

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Expression of SWI/SNF subunits BRG1 and BRM in C33A cells

Project description:We exogenously expressed the SWI/SNF ATPase catalytic subunits BRG1 and BRM in the lacking cell line C33A, and compared the differences with mock transfected cell at gene expression and alternative splicing level.

2022-03-17 | GSE140474 | GEO

Co-regulation of transcription by BRG1 and BRM, two mutually exclusive SWI/SNF ATPase subunits.

Project description:BACKGROUND:SWI/SNF is a large heterogeneous multi-subunit chromatin remodeling complex. It consists of multiple sets of mutually exclusive components. Understanding how loss of one sibling of a mutually exclusive pair affects the occupancy and function of the remaining complex is needed to understand how mutations in a particular subunit might affect tumor formation. Recently, we showed that the members of the ARID family of SWI/SNF subunits (ARID1A, ARID1B and ARID2) had complex transcriptional relationships including both antagonism and cooperativity. However, it remains unknown how loss of the catalytic subunit(s) affects the binding and genome-wide occupancy of the remainder complex and how changes in occupancy affect transcriptional output. RESULTS:We addressed this gap by depleting BRG1 and BRM, the two ATPase subunits in SWI/SNF, and characterizing the changes to chromatin occupancy of the remaining subunit and related this to transcription changes induced by loss of the ATPase subunits. We show that depletion of one subunit frequently leads to loss of the remaining subunit. This could cause either positive or negative changes in gene expression. At a subset of sites, the sibling subunit is either retained or gained. Additionally, we show genome-wide that BRG1 and BRM have both cooperative and antagonistic interactions with respect to transcription. Importantly, at genes where BRG1 and BRM antagonize one another we observe a nearly complete rescue of gene expression changes in the combined BRG/BRM double knockdown. CONCLUSION:This series of experiments demonstrate that mutually exclusive SWI/SNF complexes have heterogeneous functional relationships and highlight the importance of considering the role of the remaining SWI/SNF complexes following loss or depletion of a single subunit.

| S-EPMC5740901 | biostudies-literature

Co-regulation of transcription by BRG1 and Brm, two mutually exclusive SWI/SNF ATPase subunits

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-08-21 | GSE102561 | GEO

Expression of SWI/SNF subunits BRG1 and BRM in C33A cells

Project description:Expression of SWI/SNF subunits BRG1 and BRM in C33A cells

| PRJNA589860 | ENA

RNAi knock down of SWI-SNF subunits BRM, MOR, SNR1, OSA, PB, BAP170 and ISWI in Drosophila

Project description:RNAi knockdown of SWI-SNF subunits BRM, MOR, SNR1, OSA, PB, BAP170 and ISWI

2007-03-01 | E-TABM-169 | biostudies-arrayexpress

Cooperative and Antagonistic Transcriptional Regulation by BRG/BRM [RNA-seq]

Project description:We monitored the transcription changes associated with loss of BRG1, BRM, or both combined I HepG2 cells to understand the functional relationship between two mutually exlusive subunits of SWI/SNF

2017-08-21 | GSE102560 | GEO

Loss of the SWI/SNF ATPase subunits BRM and BRG1 drives lung cancer development.

Project description:Inactivation of Brg1 and Brm accelerated lung tumor development, shortened tumor latency, and caused a loss of differentiation. Tumors with Brg1 and/or Brm loss recapitulated the evolution of human lung cancer as observed by the development of local tumor invasion as well as distal tumor metastasis, thereby making this model useful in lung cancer studies. Brg1 loss contributed to metastasis in part by driving E-cadherin loss and Vimentin up-regulation. By changing more than 6% of the murine genome with the down-regulation of tumor suppressors, DNA repair, differentiation and cell adhesion genes, and the concomitant up-regulation of oncogenes, angiogenesis, metastasis and antiapoptosis genes, caused by the dual loss of Brg1/Brm further accelerated tumor development. Additionally, this Brg1/Brm-driven change in gene expression resulted in a nearly two-fold increase in tumorigenicity in Brg1/Brm knockout mice compared with wild type mice. Most importantly, Brg1/Brm-driven lung cancer development histologically and clinically reflects human lung cancer development thereby making this GEMM model potentially useful.

| S-EPMC5235921 | biostudies-literature

Expression data from Arabidopsis wt and ga1-3, brm-1, ga1-3/brm-1 mutants

Project description:Arabidopsis brm plants depleted in a SWI/SNF-type ATPase BRM have decreased level of endogenous gibberellins and a phenotype that in many respects resembles the phenotype of mutants with repressed GA signaling or biosynthesis, like ga1-3. ga1-3/brm double mutant showed several additive and synergistic effects. To examine whether the phenotypic traits of brm, ga1-3 and ga1-3/brm lines are reflected at the gene expression level, we compared the expression profiles of brm, ga1-3, ga1-3/brm and wild-type plants using microarray analysis. Microarray analysis was performed on total RNA isolated from shoots of 18-d-old wt, brm, ga1-3, and ga1-3/brm seedlings. Three biological replicates were examined for each genotype. Plants were grown simultaneously under the same conditions.

2013-03-08 | E-GEOD-26848 | biostudies-arrayexpress

Comparison of gene expression in control and BRG1-knockdown H358 cell lines

Project description:Transcription was assessed in the human H358 NSCLC cell line after knockdown of BRG1, one of the mutually exclusive subunits of the SWI/SNF chromatin remodeling complex, by 2 different shRNAs. One biolgical replicate of each treatment; 4 technical replicates of each treatment.

2014-09-23 | E-GEOD-58542 | biostudies-arrayexpress

Smarca4 (Brg1) is a haploinsufficient B-cell tumor suppressor that fine-tunes centrocyte cell fate decisions [ca46_atac]

Project description:SMARCA4 encodes one of two mutually-exclusive ATPase subunits in the Brg/Brm associated factor (BAF) complex that is recruited by transcription factors to drive chromatin accessibility and transcriptional activation. SMARCA4 is among the most recurrently mutated genes in human cancer, including ~30% of germinal center (GC)-derived Burkitt lymphomas. In mice, GC-specific Smarca4 haploinsufficiency cooperates with Myc over-expression to drive lymphomagenesis. Furthermore, monoallelic Smarca4 deletion drove GC hyperplasia with centroblast polarization via significantly increased rates of centrocyte recycling to the dark zone. Mechanistically, Smarca4 loss reduced the activity of transcription factors that are activated in centrocytes to drive GC-exit, including SPI1 (PU.1), IRF family and NFκB. Loss of activity for these factors phenocopied aberrant Bcl6 activity within murine centrocytes and human BL cells. Smarca4 therefore facilitates chromatin accessibility for transcription factors that shape centrocyte trajectories, and loss of fine-control of these programs biases towards centroblast cell-fate and GC hyperplasia.

2024-02-05 | GSE254902 | GEO

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