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Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE240224 | GEO | 2023/08/12

REPOSITORIES: GEO

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Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis [scRNA-seq]

Project description:In the mammalian brain, Notch signaling maintains the cortical stem cell pool and regulates the glial cell fate choice and differentiation. However, the function of Notch in regulating glial development and its involvement in tumorigenesis have not been well understood. Here, we show that Notch inactivation by genetic deletion of Rbpj in stem cells decreases astrocytes but increases oligodendrocytes with altered internal states. Interestingly, inhibiting Notch in glial progenitors does not affect cell generation but instead accelerates the growth of Notch-deprived oligodendrocyte progenitor cells (OPCs), and OPC-related glioma. We also identified a crosstalk between oligodendrocytes and astrocytes, with premyelinating oligodendrocytes secreting Bmp4, which is repressed by Notch, to upregulate GFAP expression in adjacent astrocytes. Moreover, Notch inactivation in stem cells causes a glioma subtype shift from astroglia-associated to OPC-correlated patterns, and vice versa. Our study reveals Notch's context-dependent function, promoting astrocytes and astroglia-associated glioma in stem cells and repressing OPCs and related glioma in glial progenitors.

2023-08-12 | GSE240222 | GEO

Context-dependent Regulation of Notch Signaling in Glial Development and Tumorigenesis [Bulk RNA-seq]

2023-08-12 | GSE240223 | GEO

Ets1 confers context-dependent activation of Notch signaling in T-cell leukemia

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

2020-07-07 | GSE138660 | GEO

Notch Signaling in Glial Development

Project description:Animal pole tissue explants were dissected from either untreated embryos or embryos injected with 1 ng of Notch Intracellular Domain RNA (NICD) at the two cell stage. Tissue explants were dissected and cultured until sibling embryos reached embryonic stage 20. Each array hybridization represents a biological replicate containing approximately 100 tissue explants. Expression profiles were determined using Affymetrix Xenopus Genechip 1 arrays. Keywords: repeat

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Evolution of Context Dependent Regulation by Expansion of Feast/Famine Regulatory Proteins

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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A Primate lncRNA Mediates Notch Signaling During Neuronal Development by Sequestering miRNA

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Acetylation-Dependent Regulation of Notch Signaling in Macrophages by SIRT1 Affects Sepsis Development.

Project description:SIRT1 is reported to participate in macrophage differentiation and affect sepsis, and Notch signaling is widely reported to influence inflammation and macrophage activation. However, the specific mechanisms through which SIRT1 regulates sepsis and the relationship between SIRT1 and Notch signaling remain poorly elucidated. In this study, we found that SIRT1 levels were decreased in sepsis both in vitro and in vivo and that SIRT1 regulation of Notch signaling affected inflammation. In lipopolysaccharide (LPS)-induced sepsis, the levels of Notch signaling molecules, including Notch1, Notch2, Hes1, and intracellular domain of Notch (NICD), were increased. However, NICD could be deacetylated by SIRT1, and this led to the suppression of Notch signaling. Notably, in macrophages from myeloid-specific RBP-J-/- mice, in which Notch signaling is inhibited, pro-inflammatory cytokines were expressed at lower levels than in macrophages from wild-type littermates and in RBP-J-/- macrophages, and the NF-?B pathway was also inhibited. Accordingly, in the case of RBP-J-/- mice, LPS-induced inflammation and mortality were lower than in wild-type mice. Our results indicate that SIRT1 inhibits Notch signaling through NICD deacetylation and thus ultimately alleviates sepsis.

| S-EPMC5949384 | biostudies-literature