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Notch signaling and Muller glia's regenerative response

ABSTRACT: Notch signaling and Muller glia's regenerative response

PROVIDER: PRJNA672149 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12888302_1.fastq.gz	Fastqsanger.gz
	SRR12888302_2.fastq.gz	Fastqsanger.gz
	SRR12888303_1.fastq.gz	Fastqsanger.gz
	SRR12888303_2.fastq.gz	Fastqsanger.gz
	SRR12888304_1.fastq.gz	Fastqsanger.gz

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Notch signaling and Muller glia's regenerative response

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

2021-07-31 | GSE160179 | GEO

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

Notch signaling via Hey1 and Id2b regulates Muller glia's regenerative response to retinal injury.

Project description:Zebrafish Müller glia (MG) respond to retinal injury by suppressing Notch signaling and producing progenitors for retinal repair. A certain threshold of injury-derived signal must be exceeded in order to engage MG in a regenerative response (MG's injury-response threshold). Pan-retinal Notch inhibition expands the zone of injury-responsive MG at the site of focal injury, suggesting that Notch signaling regulates MG's injury-response threshold. We found that Notch signaling enhanced chromatin accessibility and gene expression at a subset of regeneration-associated genes in the uninjured retina. Two Notch effector genes, hey1 and id2b, were identified that reflect bifurcation of the Notch signaling pathway, and differentially regulate MG's injury-response threshold and proliferation of MG-derived progenitors. Furthermore, Notch signaling component gene repression in the injured retina suggests a role for Dll4, Dlb, and Notch3 in regulating Notch signaling in MG and epistasis experiments confirm that the Dll4/Dlb-Notch3-Hey1/Id2b signaling pathway regulates MG's injury-response threshold and proliferation.

| S-EPMC8502208 | biostudies-literature

Oct4 overexpression and suppression of Notch signaling synergistically induce neurogenic competence in mammalian Muller glia.

Project description:Oct4 overexpression and suppression of Notch signaling synergistically induce neurogenic competence in mammalian Muller glia.

| PRJNA1162090 | ENA

Cis-Regulatory Accessibility Directs Muller Glial Development and Regenerative Capacity

Project description:Cis-Regulatory Accessibility Directs Muller Glial Development and Regenerative Capacity

| PRJNA565157 | ENA

ATAC-seq of Notch signaling response in RTE cells

Project description:ATAC-seq of Notch signaling response in RTE cells

| PRJNA953957 | ENA

RNA-seq of Notch signaling response in RTE cells

Project description:RNA-seq of Notch signaling response in RTE cells

| PRJNA953960 | ENA

RNA-seq of Notch signaling response in RTE cells

Project description:We report the gene expression profile of recent thymic emigrant (RTE) that are either responsive to Notch signals, or unresponsive to Notch signals during their maturation process. Notch responsiveness is controled by the expression of RBPJ, a key mediator of the Notch signaling pathway.

2023-04-12 | GSE229284 | GEO

ATAC-seq of Notch signaling response in RTE cells

2023-04-12 | GSE229283 | GEO

Notch signaling suppresses the progression of colorectal tumorigenesis

Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer. mRNAs from normal (WT, Notch-activated and Notch-inactivated) and tumor (WT, Notch-activated and Notch-inactivated) tissues were profiled.

2011-04-19 | E-GEOD-21392 | biostudies-arrayexpress

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