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BRG1 facilitates the development of porcine somatic cell nuclear transfer embryos [ATAC-Seq]

ABSTRACT: To investigate the effect of BRG1 overexpression in donor cells on the efficiency of porcine somatic cell nuclear transplantation. ATAC-seq results revealed that more open chromatin peaks at SMARCA4、NANOG、SOX2、MAP2K6、HIF1A sites were observed in the experimental group.

ORGANISM(S): Sus scrofa

PROVIDER: GSE231684 | GEO | 2023/05/10

REPOSITORIES: GEO

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BRG1 facilitates the development of porcine somatic cell nuclear transfer embryos [RNA-Seq]

Project description:To investigate the effect of BRG1 overexpression in donor cells on the efficiency of porcine somatic cell nuclear transplantation. In total, 2358 differentially expressed genes were identified by the RNA-seq, with 1336 up- and 1022 down-regulated genes in the experimental group. The up-regulated genes were mainly enriched in PI3K/AKT signaling pathway and WNT signaling pathway, and the down-regulated genes were mainly enriched in disease development.

2023-05-10 | GSE231682 | GEO

Microarray analysis of ATP-dependent chromatin remodeller BRG1/SMARCA4 mediated gene expression in primary human keratinocytes (PHEKs) after scratch wound assay.

Project description:siRNA mediated knockdown of BRG1/SMARCA4 in scratch wounded cell culture PHEKs, used to identify specific BRG1/SMARCA4 dependent gene expression programs which are initiated during immediate and early (1h and 24h) epithelial wounding. 3 human donors.

2022-12-01 | E-MTAB-12452 | biostudies-arrayexpress

Aneuploidy tolerance caused by BRG1 loss allows gain of chromosome 18 and improved fitness

Project description:Aneuploidy results in decreased cellular fitness in many different species and model systems. However, aneuploidy is commonly found in cancer cells and often correlates with aggressive growth and poor prognosis, suggesting that the impact of aneuploidy on cellular fitness is context dependent. The BRG1 (SMARCA4) subunit of the SWI/SNF chromatin remodelling complex is a tumour suppressor that is frequently lost in cancer cells. Here, we used a chromosomally stable cell line to test the effect of BRG1 loss on the evolution of aneuploidy. We find that BRG1 deletion leads to an initial loss of fitness in this cell line that improves over time. The improved fitness correlates with a gain of extra copies of chromosome 18. Notably, changes in pathways that are known to promote tolerance to aneuploidy are evident immediately upon loss of BRG1, providing an environment where karyotype changes associated with a fitness advantage can be explored. At least in some genetic backgrounds, therefore, loss of the SWI/SNF complex can contribute to tumourigenesis through tolerance of aneuploidy.

2022-03-23 | PXD014954 | Pride

BRG1 facilitates the development of porcine somatic cell nuclear transfer embryos

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

2023-05-10 | GSE231685 | GEO

Re-expression of SMARCA4/BRG1 in Small Cell Carcinoma of Ovary, Hypercalcemic Type (SCCOHT) promotes an epithelial-like gene signature through an AP-1-dependent mechanism

Project description:Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is a rare and aggressive form of ovarian cancer. SCCOHT tumors have inactivating mutations in SMARCA4 (BRG1), one of the two mutually exclusive ATPases of the SWI/SNF chromatin remodeling complex. To address the role that BRG1 loss plays in SCCOHT tumorigenesis, we performed integrative multi-omic analyses in SCCOHT cell lines +/- BRG1 re-expression. BRG1 re-expression induced a gene and protein signature similar to an epithelial cell and gained chromatin accessibility sites correlated with other epithelial originating TCGA tumors. Furthermore, AP-1 motifs were enriched at the promoters of highly upregulated epithelial genes. Using a dominant negative AP-1 cell line, we found that both AP-1 DNA binding activity and BRG1 re-expression are necessary for the gene and protein expression of epithelial genes. Our study demonstrates that BRG1 re-expression drives an epithelial-like gene and protein signature in SCCOHT cells that depends upon AP-1 activity.

2021-01-15 | PXD014134 | Pride

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

Activation of the chromatin-remodeling factor Smarca4/Brg1 cooperates with Olig2 to establish oligodendrocyte identity and control CNS myelination [ChIP-seq]

Project description:We investigate the role of Brg1 and Olig2 during oligodendrocyte differentiation by combining gene conditional knockout and next generation sequencing technology. We generate genome-wide maps of RNA polymerase II (RPolII), Brg1 (Smarca4), Olig2 and histone modifications in primary rat oligodendrocyte precursor cells (iOLs), differentiating oligodendrocytes and mature oligodendrocytes.We found that Brg1 is intensely regulated by RPolII at the initiation of oligodedrocyte differentiation. The genomic distribution of Brg1 in differentiating oligodendrocytes is pre-directed by Olig2 in iOLs. The dynamic interaction of Brg1 and chromatin is correlate with the distinct stages of gene expression during maturation. Finally, we show that Brg1 and Olig2 localization predict critical genes controling CNS myeliantion. Our study represents the first detailed analysis of genomic landscape during the oligodendrocyte development and provides a framework for further understanding of molecular mechanisms underlying oligodendrocyte lineage progression. Genomic distribution of Brg1, Olig2, RPolII and three different histone modifications in three oligodendrocyte developemtal stages were examined using primary cells by ChIP-sequencing. Spinal cord mRNA profiles of 14-day old control and Brg1c/c;Olig1-Cre mice were generated by RNA-sequencing.

2013-01-20 | E-GEOD-42447 | biostudies-arrayexpress

Activation of the chromatin-remodeling factor Smarca4/Brg1 cooperates with Olig2 to establish oligodendrocyte identity and control CNS myelination [RNA-seq]

Project description:Spinal cord mRNA profiles of 14-day-old control (Brg1c/+;Olig1-Cre) and Smarca4/Brg1 conditional knockout (Brg1c/c;Olig1-Cre) mice were generated by RNA-seq. Differential expressed genes are identified using Cuffdiff and validated with qPCR. Spinal cord mRNA profiles of 14-day old control and Brg1c/c;Olig1-Cre mice were generated by RNA-sequencing.

2013-01-20 | E-GEOD-42443 | biostudies-arrayexpress

BRG1-dependent regulation of Wnt signaling pathway during skeletal muscle differentiation

Project description:RNA-seq analysis for C2C12 myoblasts knocked down for either only-BRG1 or only-BRM or both BRG1 and BRM. Cells were treated with an siRNA SMARTpools of four oligos each targeting either BRG1 (siGENOME mouse Smarca4 pool #M-041135-01-0020) or BRM (siGENOME mouse Smarca2 pool #M-056591-00-0020) or both. Control samples were treated with non-targeting scrambled oligos (siRNA SMARTpool ON-TARGETplus scrambled non-targeting pool # D-001810-10-20). siRNA pools were purchased from Dharmacon, Horizon Discovery Ltd., USA.

2023-06-24 | GSE196283 | GEO

BRG1 loss predisposes lung cancers to replicative stress and ATR dependency

Project description:Gupta M, Concepcion CP, Fahey CG, Keshishian H, Bhutkar A, Brainson CF, Sanchez-Rivera FJ, Pessina P, Kim JY, Simoneau A, Paschini M, Beytagh MC, Stanclift C, Schenone M, Mani DR, Li C, Oh A, Li F, Hu H, Karatza A, Bronson RT, Shaw AT, Hata AN, Wong K, Zou L, Carr SA, Jacks T, Kim CF. Cancer Res 2020. Inactivation of SMARCA4/BRG1, the core ATPase subunit of mammalian SWI/SNF complexes, occurs at very high frequencies in non-small cell lung cancers. There are no targeted therapies for this subset of lung cancers, nor is it known how mutations in BRG1 contribute to lung cancer progression. Using a combination of gain- and loss-of-function approaches, we demonstrate that deletion of BRG1 in lung cancer leads to activation of replication stress responses. Single-molecule assessment of replication fork dynamics in BRG1-deficient cells revealed increased origin firing, mediated through pre-licensing protein CDC6. Quantitative mass spectrometry and co-immunoprecipitation assays showed that BRG1-containing SWI/SNF complexes interact with RPA complexes. Lastly, we show that BRG1-deficient lung cancers are sensitive to the pharmacological inhibition of ATR. These findings provide novel mechanistic insight into BRG1-mutant lung cancers and suggest that their ATR dependency can be leveraged therapeutically, and potentially expanded to BRG1- mutant cancers in other tissues.

2020-07-08 | MSV000085701 | MassIVE

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