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Transcriptional response to Notch activation in SVG-A cells

ABSTRACT: SVG-A cells are immortalized fetal astrocytes that respond to Notch signaling. We characterized the transcriptional response to Notch activation in this cell line by performing RNA-seq on cells grown on tissue culture dishes coated with JAGGED1, a Notch ligand. Differential gene expression analysis shows induction of both canonical Notch responsive genes, as well as cell-type specific Notch responsive genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE235637 | GEO | 2024/02/28

REPOSITORIES: GEO

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Notch-Jagged signaling complex defined by an interaction mosaic

Project description:The Notch signaling system links cellular fate to that of its neighbors, driving proliferation, apoptosis, and cell differentiation in metazoan organisms, whereas dysfunction leads to debilitating developmental disorders and cancers. Here we probe the molecular architecture of mammalian Notch1 full ectodomain in complex with the canonical ligand Jagged1 using cross-linking mass spectrometry (XL-MS). Our data reveals that three Jagged1 sites, C2-epidermal growth factor (EGF) 1, EGF10 and cysteine-rich domain (CRD), are in proximity to the Notch1 negative regulatory region (NRR) in the Notch1-Jagged1 full ectodomain complex. We verified direct interactions and identified additional interacting regions by quantitative-binding experiments. In addition, XL-MS and structural analysis reveal Notch1 and Jagged1 ectodomain intramolecular interactions and structural flexibility that support the formation of backfolded architectures. Together the data suggest a direct and intricate role for the different extracellular regions of Notch1 and Jagged1 in the activation and regulation of Notch1 signaling.

2021-07-08 | PXD023072 | Pride

β-cell Jagged1 is sufficient but not necessary for islet Notch activity and insulin secretory defects.

Project description:Objective Notch signaling is re-activated in β cells from obese mice, and is causal to β cell dysfunction. Notch activity is determined in part by expression of transmembrane ligand availability in a neighboring cell. We hypothesized that β cell expression of Jagged1 determines the maladaptive Notch response and resultant β cell dysfunction in obese mice. Methods We assessed expression of Notch pathway components in diet-induced obese (DIO) or leptin receptor-deficient (db/db) mice, and performed single cell RNA sequencing (scRNAseq) in islets from patients with and without type 2 diabetes (T2D). We generated and performed glucose tolerance testing in inducible, β cell-specific Jagged1 gain-of- and loss-of-function mice. We also tested effects of monoclonal neutralizing antibodies to Jagged1 in glucose-stimulated insulin secretion (GSIS) assays in isolated islets. Results Jag1 was the only Notch ligand that tracked with increased Notch activity in DIO and db/db mice. Consistently, JAG1 tracked with Notch activity in metabolically inflexible β cells enriched in patients with T2D. Neutralizing antibodies to block Jagged1 in islets isolated from DIO and db/db mice potentiated GSIS ex vivo. To demonstrate if β cell Jagged1 is sufficient to cause glucose tolerance in vivo, we generated inducible β cell-specific Jag1 transgenic mice (β-Jag1TG), which showed impaired glucose intolerance due to reduced GSIS. However, β cell-specific Jagged1 loss-of-function (β-Jag1KO) did not protect against HFD-induced insulin secretory defects or glucose intolerance. Conclusions Jagged1 is increased in islets from obese mice and in patients with T2D, and neutralizing Jagged1 antibodies lead to improved GSIS, suggesting that inhibition of Jagged1-Notch signaling may have therapeutic benefit. However, genetic loss-of-function experiments suggest that β cells are not a likely source of the Jagged1 signal.

2024-02-23 | GSE249170 | GEO

Notch signaling pathway in tooth shape variations throughout evolution

Project description:Evolutionary changes in vertebrates are linked to genetic alterations that often affect tooth-crown shape, which is a criterion of speciation events, especially in mammals. The Notch pathway is highly conserved between species and controls morphogenetic processes in most developing organs, including teeth. Epithelial loss of the Notch-ligand Jagged1 in developing mouse molars affects the location, size and interconnections of their cusps that lead to minor tooth-crown shape modifications convergent to those observed along Muridae evolution. RNA sequencing analysis revealed that these alterations are due to the modulation of more than 2000 genes and that Notch signaling is a hub for significant morphogenetic networks, such as Wnts and Fibroblast Growth Factors. The modeling of these tooth-crown changes in mutant mice, via a three-dimensional metamorphosis approach, allowed prediction of how Jagged1-associated mutations in humans could affect the morphology of their teeth. These results shed new light on Notch/Jagged1-mediated signaling as one of the crucial components for dental variations in evolution.

2023-03-17 | GSE198920 | GEO

The downstream molecules of Notch signaling in vascular endothelial cell senescence

Project description:To further investigate the mechanism how the decline in Notch signaling induces premature senescence in endothelial cells, we performed microarray analysis and identified Id1 nd DUSP1 as the downstream molecules of Notch pathway. In quantitative PCR and western blot analyses, the expression level of Id1 and DUSP1 increased in Notch1 over-expressing endothelial cells and decreased in knockdown similar to the result of microarray. The gene expression of human unbilical endothelial vein cells (HUVEC) infected with retroviral vectors encoding Jagged1, Jagged1-shRNA, or Notch1-shRNA. HUVEC infected with empty vector was used as a control. In each genotypes, three independent lines at passage 8 were performed.

2012-08-28 | E-GEOD-40403 | biostudies-arrayexpress

Transcription profiling of human SVG-A glial cells and SVGR2 glial cells

Project description:SVGR2 cells are glial cells which are derived from SVG-A cells. They were created by subjecting SVG-A cells to multiple rounds of lytic infection by the human polyomavirus JCV. SVGR2 cells are the cells that survived this process and are resistant to JCV infection. This experiment was designed to identify gene expression differences that may be responsible for SVGR2 resistance to JCV. Experiment Overall Design: SVG-A and SVGR2 cells are transformed cell lines. To eliminate gene expression differences that may have occurred due to genetic instability of these cell lines three subclones of each of the cell lines were created and used as a triplicate in the comparison. Total RNA was extracted from cells that had been left at 100% confluency for one day using the Qiagen RNeasy kit. cDNA was hybridized to the Affymetrix Human GeneChips U133A or U133B according to Affymetrix gudielines.

2008-11-07 | E-GEOD-7819 | biostudies-arrayexpress

Comparison of gene expression in SVG-A glial cells and SVGR2 glial cells

2007-05-25 | GSE7819 | GEO

Effect of depletion of Notch signaling genes in C2C12 cells on the activation of Notch pathway activity in response to stimulation by plated ligand

Project description:To obtain a Notch-depleted base cell line into which we could integrate specific ligands or receptors for quantitative analysis of Notch signaling interactions, we conducted 2 rounds of transfection with RNPs (ribonucleoproteins) consisting of gRNAs targeting Notch2 and Jagged1 complexed with Cas9 protein. After antibiotic selection and screening of monoclonal colonies, we obtained the C2C12-Nkd clone, which showed loss of Notch2 protein and Jag1 transcript.

2023-06-02 | GSE233573 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [RNA-Seq]

Project description:We decribe the accessible chormatin landscape in RAS-induced (RIS) and NOTCH induced senescence (NIS) using ATAC-seq. By expressing active NOTCH (N1ICD) in the context of RIS, we find that N1ICD antagonises the formation of accessible regions in RIS. By performing co-cultures, we demonstrate that cells expressing a NOTCH1 ligand, JAGGED1, can antagonise the formation of RIS specific accessible regions.

2018-04-24 | GSE113060 | GEO

NOTCH-mediated non-cell autonomous regulation of chromatin structure during senescence [ATAC-Seq]

Project description:We describe the accessible chormatin landscape in RAS-induced (RIS) and NOTCH induced senescence (NIS) using ATAC-seq. By expressing active NOTCH (N1ICD) in the context of RIS, we find that N1ICD antagonizes the formation of accessible regions in RIS. By performing co-cultures, we demonstrate that cells expressing a NOTCH1 ligand, JAGGED1, can antagonize the formation of RIS specific accessible regions.

2018-04-24 | GSE103588 | GEO

SVG cells infected with Zika virus for 24, 48 and 72 hr post infection

Project description:Transcriptional profiling of human astrocyte cells (SVG) infected with Zika virus. Goal was to identify temporal changes in gene expression post infected by Zika virus.

2017-10-13 | GSE89915 | GEO

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