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Compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells by ATAC-Seq

ABSTRACT: Compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells by ATAC-Seq

PROVIDER: PRJNA475576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7290301_1.fastq.gz	Fastqsanger.gz
	SRR7290301_2.fastq.gz	Fastqsanger.gz
	SRR7290302_1.fastq.gz	Fastqsanger.gz
	SRR7290302_2.fastq.gz	Fastqsanger.gz

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Compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells by ATAC-Seq

Project description:Transposase-accessible chromatin using sequencing (ATAC-seq) assay was performed to compare chromatin open regions (OCRs) between PTEN-KD and PTEN/BRG1-KD 22RV-1 cells. Ablation of BRG1 in PTEN-depleted cells preferentially led to the reductions of OCR at enhancers, but not promoter regions.

2019-01-14 | GSE115617 | GEO

Transcriptome analysis of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation

Project description:We conduct transcriptome comparison of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation to gain genomic insights on the biological processes that BRG1 is involved in depend on PTEN deletion. Through unsupervised cluster analysis of differentially expressed genes (DEGs), we found the expressions of 5489 genes were significantly altered in PTEN/BRG1 double knockdown cells, whereas they remained consistent or opposite pattern in control, BRG1-KD and PTEN-KD cells. Differential principal component analysis (PCA) suggested ablation of BRG1 in PTEN-depleted cells forced the cells undergoing a distinct transcriptome as compared to the others. In keeping with these findings, KEGG-DEGs relationship network indicated BRG1 loss in PTEN-deficient cells significantly altered the process related to “Prostate cancer”, “Cell cycle”, “Cell motility” and etc.

2019-01-14 | GSE115616 | GEO

BRG1 occupancy profiling by high throughput sequencing from control and PTEN knockdown 22RV-1 cells

Project description:To identify the downstream targets and pathways mediated by BRG1, chromatin immunoprecipitation followed by sequencing (ChIP–seq) was performed in control and PTEN-knockdown 22RV-1 cells. Total 6279 genes showed the enhanced BRG1 occupancies in PTEN-knockdown cells as compared to that in control cells. Genome-wide analysis revealed that PTEN loss lead to increase BRG1 intervals specifically localized at enhancers, but not distal promoter regions. We therefore reasoned ablation of BRG1 might impair enhancer configurations in PTEN-deficient cells.

2019-01-14 | GSE115615 | GEO

Open chromatin sites identified in wildtype and Brg1-cko neurons in basal and depolarized conditions [ATAC-seq]

Project description:ATAC-seq analyses examined open chromatin regions in of wildtype and Brg1-cko neurons in basal and depolarized conditions.

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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.

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PTEN inhibition dedifferentiates long-distance axon-regenerating intrinsically photosensitive retinal ganglion cells and upregulates mitochondria-associated DYNLT1A and LARS2

Project description:The central nervous system (CNS) projection neurons fail to spontaneously regenerate injured axons. Targeting the developmentally regulated genes in order to reactivate embryonic intrinsic axon growth capacity, or targeting tumor suppressor genes such as Pten, promote axon regeneration in a subset of injured retinal ganglion cells (RGCs). The subset of RGCs that regenerate axons in response to inhibition of Pten was narrowed-down to the Opn4+ intrinsically photosensitive (ip) and α subtypes of RGCs. Here, we used single cell RNA-sequencing (scRNA-seq) to investigate why only a subset of injured RGCs regenerate axons in response to Pten knockdown (KD), and to characterize the relationship between axon regeneration promoted by targeting Pten and the developmental decline in intrinsic axon growth capacity. We found that, only the most similar to embryonic state ipRGC subtypes C33 and C40 regenerated axons in response to Pten KD, which dedifferentiated them even further towards an embryonic state. We also found that genes downstream of Pten KD, specifically in the RGCs that regenerated axons, include mitochondria-associated developmentally regulated and non-developmentally regulated Dynlt1a and Lars2, respectively, which promoted axon regeneration on their own. Overall, we show that injury itself reverts transcriptome towards an embryonic state only in some neuronal subtypes and not sufficiently close to embryonic state to confer response to Pten KD, whereas certain mature neuronal subtypes are similar to embryonic state even without injury, which primes them to regenerate axons in response to Pten KD, that dedifferentiates them further towards an embryonic state and upregulates mitochondria-associated Dynlt1a and Lars2.

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SWI/SNF Chromatin Remodeling Factor BRG1 is Synthetic Required for PTEN-deficient Prostate Cancer

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Dynamic BRG1 Recruitment During T Helper Differentiation And Activation Reveals Distal Regulatory Elements

Project description:We found binding of the remodeling protein BRG1 was programmed by lineage and activation signals. BRG1 binding was positively correlated with gene activity at protein-coding and miRNA genes. BRG1 binding was found at promoters and distal regions, including known and novel distal regulatory elements. Distal BRG1 binding correlated with expression, and novel distal sites possessed enhancer activity, suggesting a general role for BRG1 in long-distance gene regulation. Together, these findings suggest BRG1 interprets differentiation and activation signals and plays a causal role in gene regulation, chromatin structure, and cell fate. Our findings indicate BRG1 binding is a useful marker for identifying cis-regulatory regions in protein-coding and miRNA genes. Compare BRG1 binding in T helper subsets genome wide; Naïve, resting Th1, resting Th2, Stimulated Th1, Stimulated Th2, Stimulated Th17, compared to input DNA as negative control

2011-03-01 | E-GEOD-23719 | biostudies-arrayexpress

PTEN loss and expression of the TMPRSS2/ERG fusion gene transform prostatic epithelial cells via enhanced FGF signaling

Project description:To determine if ERG expression and PTEN loss were sufficient to transform prostate epithelial cells we constructed cell lines with expression of the TMPRSS2/ERG fusion gene (TE), stable knockdown of PTEN with shRNA (PTEN KD) or both alterations (PTEN KD/TE) using the PNT1A cell line. To determine what gene expression changes are associated the phenotypic changes between the cell line experimental groups, we carried expression microarray studies using Agilent 60K expression microarrays. RNAs from all four cell lines were analyzed in duplicate and probes with ≥ 1.4-fold or ≤0.7-fold relative to control cells identified. Our results demonstrated that PTEN loss and expression of the TMPRSS2/ERG fusion gene transform prostatic epithelial cells via enhanced FGF signaling.

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Reverse Phase Protein Array (RPPA) profiling of cell signaling events in 468 cells induced by PTEN overexpression or PTEN-Long overexpression

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