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Synergistic activation of RARb and RARg-driven programs restores cell-types specialization during stem cell differentiation

ABSTRACT: Synergistic activation of RARb and RARg-driven programs restores cell-types specialization during stem cell differentiation

PROVIDER: PRJNA842391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19403336_1.fastq.gz	Fastqsanger.gz
	SRR19403336_2.fastq.gz	Fastqsanger.gz
	SRR19403337_1.fastq.gz	Fastqsanger.gz
	SRR19403337_2.fastq.gz	Fastqsanger.gz
	SRR19403338_1.fastq.gz	Fastqsanger.gz

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Synergistic activation of RARb and RARg-driven programs restores cell-types specialization during stem cell differentiation

Project description:How cells respond to different external cues to develop along defined cell lineages composing complex tissues is a major question in systems biology. In this study, we studied the role of synthetic agonists targeting specific Retinoic acid receptors (RARs) on activating major gene regulatory wires driving cell specialization during nervous tissue formation issued from P19 stem cells. Specifically, we have revealed that the synergistic activation of the RAR and RAR nuclear receptors by their cognate ligands (BMS641 or BMS961) induce neuronal maturation, inlcuding specialized neuronal subtypes as well as to astrocytes and oligodendrocyte precursors. With the help of Rar-null mutant lines, combined with the use of RAR-specific agonists, global transcriptome mapping and an in-silico modeling of transcription regulatory signalling propagation, we have highlighted major gene programs essential for optimal neuronal cell specialization. Overall, this study provides a systems biology view of the gene programs behind the previously observed redundancy between RAR receptors, paving the way for their potential use for directing cell specialization during nervous tissue formation.

2022-11-10 | GSE204816 | GEO

wnt1-induced mammary tumor from Rarb KO mice vs. those from Rarb wt (control)

Project description:Previously we have demonstrated that inactivation of retinoic acid receptor beta (Rarb) in the mouse results in a protective effect against ErbB2-induced mammary gland tumorigenesis although Rarb has been reported as a tumor suppressor before. In the current study, we further confirmed that ablation of Rarb has a very similar impact on Wnt1-induced mammary gland tumorigenesis as those on ErbB2-induced mammary gland tumorigenesis. Nevertheless, the mechanisms by which Rarb confers its effects on tumor progression is quite different although both involving in tumor microenvironment (TME) remodeling. In the Wnt1 tumors, ectopic wnt1 produced by malignant luminal cells activates nearby stromal cells by a paracrine manner. In return, the stromal cells secreted IGF1 to regulate the growth of tumor cells. There is a need of Rarb expression in this interaction. Deletion of Rarb inhibits both wnt1/β-catenin signaling and IGF1/Akt axis in the myoepithelial tumor cells which results in the suppression of epithelial-mesenchymal transition (EMT) in these tumors. Since wnt1 tumors resemble basal-like breast cancer with a poor clinical prognosis in which EMT is one of the most important way for tumor cells to survive against standard treatment and to go to metastasis, we propose that (1) the stromal gene expression signature of Rarb ablation in wnt1 tumors could have some clinical value in predicting the breast cancer outcome; and (2) Rarb antagonist might be a potential therapeutic strategy in EMT-driven aggressive cancers such as basal-like breast cancer.

2014-10-23 | GSE56391 | GEO

Identifying RARG fusions or PML-RARA binding genes or analysis the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

Project description:To understand how RARG fusion proteins regulate their target genes in the hematopoietic system, we overexpressed fusions or PML-RARA in hCD34+ cells and identified target genes that are regulated by RARG fusions. We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we dected the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) associated with RARG fusions binding in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

2024-10-16 | GSE275303 | GEO

wnt1-induced mammary tumor from Rarb KO mice vs. those from Rarb wt (control)

2014-10-23 | E-GEOD-56391 | biostudies-arrayexpress

RARb and Huntington Disease

Project description:RARb and Huntington Disease

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RARG fusion genes

Project description:RARG fusion genes

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Analysis of the chromatin accessibility in CPSF6-RARG or NUP98-RARG overexpressing hCD34+ cells compared to control hCD34+ cells using ATAC-seq.

Project description:We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we defined the chromatin accessibility using ATAC-seq assay in human CD34+ (hCD34+) cells with or without CPSF6::RARG or NUP98::RARG overexpression.

2024-10-16 | GSE275304 | GEO

The gene expression profiles of leukemia cells isolated from spleens of CreMx-1;CPSF6-RARG mice and Wt1F/+CreMx-1;CPSF6-RARG mice

Project description:We found that CPSF6-RARG fusion gene drives the aberrant expansion of HSCs and progenitor cells, which may lead to a preleukemic phenotype. Moreover, wt1 haploinsufficiency cooperates with RARG fusions to induce AML. To investigate the mechanism by which Wt1 haploinsufficiency cooperates with RARG fusion overexpression to induce AML in vivo, we analyzed the gene expression profiles of leukemia cells isolated from CreMx-1;CPSF6-RARG mice and Wt1F/+CreMx-1;CPSF6-RARG mice through RNA-seq.

2024-10-15 | GSE243415 | GEO

RNA-sequencing experiments comparing P0 control and RXRG/RARb double mutants frontal cortex

Project description:To understand the functional significance of RA signaling through the RXRG/RARB heterodimer in the developing cortex, we performed RNA-seq experiments comparing different regions of the P0 mouse frontal cortex (mPFC, secondary motor cortex (MOs)/ primary motor cortex (MOp), and OFC ) in Rarb and Rxrg dKO and WT littermate controls.

2021-01-01 | GSE142851 | GEO

The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression VI

Project description:Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RARG), are commonly reduced in prostate cancer (PCa). Therefore we sought to establish the cellular and gene regulatory consequences of reduced RARG expression, and determine RARG regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RARG levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RARG cistrome which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RARG to regulate androgen signaling, RARG knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RARG down-regulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RARG expression and function. Capture of the miR-96 targetome by biotin-miR96 identified that RARG and a number of RARG interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RARG target genes (e.g. SOX15) that significantly associated with worse disease free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p=0.015). In summary, miR-96 targets a RARG network to govern AR signaling, PCa progression and disease outcome. ChIP-seq: RWPE-1-BAC-RARG-EGFP non-malignant, immortalized cell line infected with BAC-RARG-EGFP, +/- 10nM CD437 for 2 hours

2018-07-20 | GSE117179 | GEO

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