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Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage [RNA-seq]

ABSTRACT: Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage [RNA-seq]

PROVIDER: PRJNA1065434 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27563600_1.fastq.gz	Fastqsanger.gz
	SRR27563600_2.fastq.gz	Fastqsanger.gz
	SRR27563601_1.fastq.gz	Fastqsanger.gz
	SRR27563601_2.fastq.gz	Fastqsanger.gz
	SRR27563602_1.fastq.gz	Fastqsanger.gz

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Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage [RNA-seq]

Project description:Copper (Cu)-binding transcription factors are emerging as important regulators of gene expression during skeletal muscle differentiation. Our group has shown that the classic Metal Transcription Factor 1, MTF1, works cooperatively with the myogenic factor MyoD to promote skeletal muscle differentiation and ensure viability of murine primary myoblasts. Preliminary evidence showed that MTF1 interacts with members of the mammalian SWItch/Sucrose Non-Fermentable (mSWI/SNF) family of ATP-dependent chromatin remodeling enzymes to promote differential gene expression in proliferating and differentiating myoblasts. mSWI/SNF complexes are assembled into three major subfamilies that are distinguished by the presence of mutually exclusive subunits: cBAF (canonical BRG1 or BRM-Associated Factor), PBAF (Polybromo containing BAF), or ncBAF (non-canonical BAF). The mechanisms by which each subfamily contributes to the establishment or function of specific cell lineages are poorly understood. We determined the contributions of the BAF, ncBAF, and PBAF complexes to myoblast proliferation, differentiation, and metal homeostasis via knock-down (KD) of a distinguishing subunit of each complex (Baf250A, Brd9, and Baf180, respectively). Biochemical, molecular and RNA-seq analyses showed that Baf250A KD reduced myoblast proliferation rate and differentiation. Brd9 KD resulted in a minor proliferation defect and a delay in myogenesis. KD of Baf180 and other PBAF-specific subunits did not impact proliferation or differentiation but affected the maintenance of metal homeostasis in myoblasts. The data support a model for differential roles and interactions between MTF1 and a novel category of Cu-binding transcription factors and the SWI/SNF enzymes in the development and homeostasis of the skeletal muscle lineage.

2024-10-26 | GSE253377 | GEO

Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage [CUT&RUN]

2024-10-26 | GSE253376 | GEO

Differential requirements for the BAF and ncBAF subfamilies of the mammalian SWI/SNF chromatin remodeling enzymes during skeletal muscle differentiation.

Project description:Subunit proteins BAF250a and Brd9 are specific to mammalian SWI/SNF subfamilies BAF and ncBAF respectively. We have performed RNA-seq analysis for C2C12 myoblasts stably knocked down for each subunits using specific shRNA constructs. C2C12 cells stably transfected with non-targeting scrambled shRNA construct were used as controls.

2023-07-10 | GSE196281 | GEO

Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage

Project description:Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage

| PRJNA1065431 | ENA

Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage [CUT&RUN]

Project description:Differential roles of copper-binding transcription factors and the subfamilies of the SWI/SNF complex in the transcriptional regulation of the skeletal muscle lineage [CUT&RUN]

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siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

Genome-wide profile of the SWI/SNF chromatin remodeling complex

Project description:A systems understanding of nuclear organization and events is critical for determining how cells divide, differentiate and respond to stimuli and for identifying the causes of diseases. Chromatin remodeling complexes such as SWI/SNF have been implicated in a wide variety of cellular processes including gene expression, nuclear organization, centromere function and chromosomal stability, and mutations in SWI/SNF components have been linked to several types of cancer. To better understand the biological processes in which chromatin remodeling proteins participate we globally mapped binding regions for several components of the SWI/SNF complex throughout the human genome using ChIP-Seq. SWI/SNF components were found to lie near regulatory elements integral to transcription (e.g. 5M-bM-^@M-^Y ends, RNA Polymerases II and III and enhancers) as well as regions critical for chromosome organization (e.g. CTCF, lamins and DNA replication origins). To further elucidate the association of SWI/SNF subunits with each other as well as with other nuclear proteins we also analyzed SWI/SNF immunoprecipitated complexes by mass spectrometry. Individual SWI/SNF factors are associated with their own family members as well as with cellular constituents such as nuclear matrix proteins, key transcription factors and centromere components implying a ubiquitous role in gene regulation and nuclear function. We find an overrepresentation of both SWI/SNF-associated regions and proteins in cell cycle and chromosome organization. Taken together the results from our ChIP and immunoprecipitation experiments suggest that SWI/SNF facilitates gene regulation and genome function more broadly and through a greater diversity of interactions than previously appreciated. ChIP-Seq analysis of the SWI/SNF subunits Ini1, Brg1, BAF155 and BAF170 in HeLa S3 cells

2011-01-10 | E-GEOD-24397 | biostudies-arrayexpress

Diverse roles and interactions of the SWI/SNF chromatin-remodeling complex revealed using global approaches

Project description:This SuperSeries is composed of the following subset Series: GSE24382: Lamin binding profiles in the ENCODE regions GSE24397: Genome-wide profile of the SWI/SNF chromatin remodeling complex Refer to individual Series

2011-01-10 | E-GEOD-24398 | biostudies-arrayexpress

ARID-DNA interactions are essential for SWI/SNF function

Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of these complexes, physiological roles for this domain remain undefined. We screened an N-ethyl-N-nitrosurea (ENU) mutagenized library for ARID domain point mutations and generated an Arid1a/Baf250a hypomorphic allele. The mutant ARID1a (V1068G) protein is stably expressed at wild-type levels, and it is capable of assembling into a SWI/SNF complex with in vitro mononucleosome disruption activity. However, its capacity to bind DNA is lost. Consistent with defective DNA binding, mutant protein occupancy at known SWI/SNF target genes is decreased. Loss of DNA binding is associated with concurrent changes in SWI/SNF target gene expression. Mutant embryos manifest heart defects, fail to establish proper yolk sac vasculature, and exhibit hemorrhaging. As a result of these phenotypes, mutant embryos fail to establish proper circulation, culminating in ischemic arrest in utero between days 9.5 and 11.5. These data support a role for ARID1a-containing, BAF-A complexes in heart and extraembryonic vascular development, and indicate the ARID domain of ARID1a is essential in this regard. Hence, intrinsic ARID subunit-DNA interactions are required for normal SWI/SNF function in vivo. Four-condition experiment, wild-type vs Baf250a/Arid1a^V1068G/V1068G yolk sacs isolated at E8.5 and E9.5. Biological replicates: 3 per condition.

2012-01-15 | E-GEOD-32116 | biostudies-arrayexpress