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Single cell RNA‐seq in the sea urchin embryo show marked cell‐type specificity in the Delta/Notch pathway

ABSTRACT: Single cell RNA‐seq in the sea urchin embryo show marked cell‐type specificity in the Delta/Notch pathway

PROVIDER: PRJNA554833 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9693264.fastq.gz	Fastqsanger.gz
	SRR9693265.fastq.gz	Fastqsanger.gz
	SRR9693266.fastq.gz	Fastqsanger.gz

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Similar Datasets

Single cell RNA-seq in the sea urchin embryo show marked cell-type specificity in the Delta/Notch pathway.

Project description: Not available

| S-EPMC6690749 | biostudies-literature

Single cell RNA‐seq in the sea urchin embryo show marked cell‐type specificity in the Delta/Notch pathway

Project description:Overall, we conclude that single cell RNA‐seq analysis in this embryo is revealing of the cell types present during development, of the changes in the gene regulatory network resulting from inhibition of various signaling pathways, and of the selectivity of these pathways in influencing developmental trajectories.

2019-07-17 | GSE134350 | GEO

ChIP-chip from DmD8 cells with Twist antibodies after 30 minutes Notch activation

Project description:The transcription factor Twist is a critical cooperating factor that confers transcriptional specificity to the Notch pathway in muscle progenitor cells (DmD8) ChIP analysis of Twi show that Twist binding is significantly enriched in Notch responsive region in DmD8 cells 3 replicates of Twist ChIP after30 min. Notch activation.

2010-07-27 | E-GEOD-22650 | biostudies-arrayexpress

Non-visual photoreceptive brain specification in sea urchin larvae

Project description:We employed the Western Pacific model sea urchin, Hemicentrotus pulcherrimus, as our experimental system to establish a comprehensive single-cell RNA sequencing (scRNA-seq) data atlas. Our primary objective was to document stage-specific gene expression profiles during the normal developmental progression, ranging from 24 to 96 hours post-fertilization. Our particular focus lay on neurogenesis, a pivotal process occurring in the latter stages of sea urchin development. To elucidate the regulatory mechanisms governing neurogenesis, we utilized pharmacological interventions targeting the Delta-Notch signaling pathway, a central regulator of this process. By perturbing the pathway's lateral inhibition from 16 hours post-fertilization, we aimed to identify gene sets typically suppressed during neurogenesis. Subsequent to the inhibition, we observed a notable upregulation of neurogenic genes and a concurrent expansion in the cellular population expressing these genes, starting from the 24-hour time point. In addition, the processed Seurat objects (RDS files), stratified by developmental stage, experimental condition, and sample, are available through the HpHase portal (https://cell-innovation.nig.ac.jp/Hpul/).

2025-10-08 | GSE265747 | GEO

sea urchin metagenome

Project description:Sea urchin microbiome

| PRJDB12341 | ENA

ChIP-chip from DmD8 cells with Twist antibodies after 30 minutes Notch activation

2010-07-28 | GSE22650 | GEO

Notch

Project description:Notch

| PRJNA988118 | ENA

SHOW-Me

Project description:SHOW-Me

| PRJNA685236 | ENA

Notch Signaling Enhances Bone Regeneration in the Zebrafish Mandible

Project description:Loss or damage to the mandible due to trauma, treatment of oral malignancies, and other diseases is currently treated using bone grafting techniques that suffer from numerous shortcomings and contraindications. Zebrafish naturally heal large injuries to their mandibular bone, and thus offer an opportunity to understand how to boost intrinsic healing ability. Using a novel her6:mCherry Notch reporter, we show that canonical Notch signaling is induced during the initial stages of cartilage callus formation in both mesenchymal cells and chondrocytes. We also show that modulation of Notch signaling during the initial postoperative period results in lasting changes to regenerate bone quantity one month later. Notch signaling is required for mandibular bone healing, as pharmacological inhibition of Notch signaling blocks cartilage callus formation and results in non-union. Conversely, conditional transgenic activation of Notch signaling accelerates regenerative ossification. Mechanistically, we report that postoperative Notch signaling regulates multiple phases of chondroid regeneration and patterns callus metabolic landscape. Given conserved functions of Notch signaling in bone repair across vertebrates, we propose that targeted activation of Notch signaling during the early phases of bone healing may have therapeutic value.

2022-03-07 | PXD027280 | Pride

Role of Notch signaling pathway in urothelial cancer

Project description:The Notch signaling pathway controls cell fates through interactions between neighboring cells by positively or negatively affecting, in a context-dependent manner, processes of proliferation, differentiation, and apoptosis1. It has been implicated in human cancer both as an oncogene and a tumor suppressor2. Here we report, for the first time, novel inactivating mutations in the Notch pathway components in over forty percent of the human bladder cancers examined. Bladder cancer is the fourth most commonly diagnosed malignancy in the US male population3. Thus far, driver mutations in the FGFR3 and less commonly RAS proteins have been identified4,5. We show that Notch activation in bladder cancer cells suppresses proliferation both in vitro and in vivo by directly upregulating dual specificity phosphatases (DUSPs), thus reducing ERK1/2 phosphorylation. In mouse models, genetic inactivation of Notch signaling leads to ERK1/2 phosphorylation resulting in tumorigenesis in the urinary tract. In recent years, the tumor suppressor role of Notch has been recognized by loss-of-function mutations identified in myeloid cancers6 as well as squamous cell carcinomas of the skin, lung7, and the head and neck8,9. Of the 4 Notch receptors (N1-4), only N1 and 2 have been implicated in human cancer. two biological replicates from normal and tumor urothelial tissue were hybridized on Affymetrix mm 430 2.0 chips

2014-07-01 | E-GEOD-54589 | biostudies-arrayexpress

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