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Regulating lineage progression of cortical neural stem cells by extrinsic signaling molecule SHH [single-cell RNA-seq]

ABSTRACT: Regulating lineage progression of cortical neural stem cells by extrinsic signaling molecule SHH [single-cell RNA-seq]

PROVIDER: PRJNA591016 | ENA |

REPOSITORIES: ENA

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Regulating lineage progression of cortical neural stem cells by extrinsic signaling molecule SHH [bulk RNA-seq]

Project description:Regulating lineage progression of cortical neural stem cells by extrinsic signaling molecule SHH [bulk RNA-seq]

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Regulating lineage progression of cortical neural stem cells by extrinsic signaling molecule SHH [single-cell RNA-seq]

Project description:Purpose:To asses changes in gene expression profiles of single cell from the E16.5 wild type littermate controls cortex, and ShhN IUE (ShhN palsmid were electroporated to wild type mice cortex at E13.5 and the cortex were dissected at E16.5) mice. Methords: E16.5 wild type and ShhN-IUE cortices were carefully dissected under a fluorescent stereoscope, and incubated in 4 ml of papain solution for 20 min at 37℃, The cortical tissues were gently triturated, filtered through a 40 mm strainer, and washed with HBSS to obtain the single cell suspension. The Chromium droplet-based sequencing platform (10X Genomics) was used to generate scRNA-seq libraries, following the manufacturer’s instructions. The cDNA libraries were purified, quantified using Agilent 2100 Bioanalyzer, and sequenced on the Illumina Hiseq4000 Results: 7834 cells (2368 median genes per cell) captured for the Control cortex. And 8538 cells with 2422 median genes per cell captured for Shh-IUE mice.

2020-02-19 | GSE140816 | GEO

Cortical Neural Stem Cell Lineage Progression Is Regulated by Extrinsic Signaling Molecule Sonic Hedgehog

Project description:Cortical Neural Stem Cell Lineage Progression Is Regulated by Extrinsic Signaling Molecule Sonic Hedgehog

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Regulating lineage progression of cortical neural stem cells by extrinsic signaling molecule SHH [bulk RNA-seq]

Project description:Purpose:To asses changes in gene expression profiles from the P0 wild type littermate controls cortex, hGFAP-Cre, SmoM2f/+ mice cortex and ShhN IUE (ShhN palsmid were electroporated to wild type mice cortex at E13.5 and the cortex were dissected at P0) mice. Methords:Total RNA was isolated and sequenced using an illumina high-seq 2500. Raw data was analyzed using TopHat. Genes were considered significantly changed whicn perform fold-change>=2 and P value <= 0.05 Results: Compared to controls, 2466 genes were significantly down-regulated, and 5289 genes were up regulated in the RNA expression level of the SmoM2 mice; 3492 genes were significantly down-regulated, and 3577 genes were up regulated in the RNA expression level of the cortex of ShhN IUE mice.

2020-02-19 | GSE138878 | GEO

mRNA-seq of neuronal compartments in shRNA-mediated + small-molecule knockdown of Mettl3 in mouse primary cortical neurons (mPCN)

Project description:To study the effect of m6A modifications on subcellular mRNA localization we depleted m6A writer Mettl3 with shRNA and small molecule from mouse primary cortical neurons (mPCN) and sequenced neuritic and somatic compartments in parallel with scrambled shRNA control.

2023-07-12 | E-MTAB-11570 | biostudies-arrayexpress

ERK signaling expands mammalian cortical radial glial cells and extends the neurogenic period

Project description:The molecular basis for cortical expansion during evolution remains largely unknown. Here, we report that fibroblast growth factor (FGF)-extracellular signal-regulated kinase (ERK) signaling promotes the self-renewal and expansion of cortical radial glial (RG) cells. Furthermore, FGF-ERK signaling induces bone morphogenic protein 7 (Bmp7) expression in cortical RG cells, which increases the length of the neurogenic period. We demonstrate that ERK signaling and Sonic Hedgehog (SHH) signaling mutually inhibit each other in cortical RG cells. We provide evidence that ERK signaling is elevated in cortical RG cells during development and evolution. We propose that the expansion of the mammalian cortex, notably in human, is driven by the ERK-BMP7-GLI3R signaling pathway in cortical RG cells, which participates in a positive feedback loop through antagonizing SHH signaling. We also propose that the relatively short cortical neurogenic period in mice is partly due to mouse cortical RG cells receiving higher SHH signaling that antagonizes ERK signaling.

2023-08-09 | GSE240381 | GEO

Olig2 targetome in SHH subgroup of medulloblastoma

Project description:Several basic helix-loop-helix (bHLH) transcription factors are upregulated in Sonic Hedgehog subgroup of medulloblastoma (SHH MB). Olig2, a neural bHLH transcription factor known to regulate differentiation of neural cell populations, is broadly expressed in mouse models of SHH MB. ChIP-Seq of Olig2 revealed its binding to a large number of sites near genes known to promote SHH MB tumorigenesis, suggesting a potential role for Olig2 in regulating transcriptional programme of MB.

2024-03-23 | GSE103824 | GEO

AMPK attenuates SHH subgroup medulloblastoma growth and metastasis by inhibiting NF-kB activation

Project description:Background: Medulloblastoma (MB) is one of the most common malignant pediatric brain tumors. Metastasis and relapse are the leading causes of death in MB patients. The initiation of the SHH subgroup of MB (SHH-MB) is due to the aberrant activation of Sonic Hedgehog (Shh) signaling. However, the mechanisms for its metastasis are still unknown. Results: AMP-dependent protein kinase (AMPK) restrains the activation of Shh signaling pathway, thereby impeding the proliferation of SHH-MB cells. More importantly, AMPK also hinders the growth and metastasis of SHH-MB cells by regulating NF-kB signaling pathway. Furthermore, Vismodegib and TPCA-1, which block the Shh and NF-kB pathways, respectively, synergistically restrained the growth, migration, and invasion of SHH-MB cells. Conclusions: This work demonstrates that AMPK functions through two signaling pathways, SHH-GLI1 and NF-kB. AMPK-NF-kB axis is a potential target for molecular therapy of SHH-MB, and the combinational blockade of NF-kB and Shh pathways confers synergy for SHH-MB therapy.

2023-07-01 | GSE218076 | GEO

H3K27ac in WT and Shh-/-, and Shh-/-;Gli3-/- E10.5 limb buds

Project description:Purpose: The response to Hedgehog signaling in the limb is driven by GLI bound enhancers. While most Hh targets in the developing limb bud appear to be regulated by the activity of GLI-repressor, the role of GLI activator in this regulation is unclear. Here we assess the roles of GLI activator and repressor in regulating H3K27ac to activate their enhancers. Methods: ChIP-seq was performed in Embryonic day 10.5 mouse limb buds from WT, Shh-/- and Shh-/-Gli3-/- embryos Results: We found that most GLI binding regions can be activated in the absence of both GLI activator and repressor, while a small subset require GLI activator for activity. These indicate that most GLI enhancers in the limb are regulated by GLI repression.

2020-01-21 | GSE133712 | GEO

Directed differentiation of human pluripotent stem cells into cortical interneurons

Project description:Here we demonstrate the highly efficient derivation of human cortical interneurons in a NKX2.1::GFP hESC reporter line. Manipulating the timing of SHH activation yields three distinct GFP+ populations with specific transcriptional profiles, neurotransmitter phenotypes and migratory behaviors. Total RNA was isolated at day 18 of differentiation from FACS sorted NKX2.1::GFP+ cells from three varying differentiation conditions and a “No SHH” condition (no sonic hedgehog treatment) that did not contain any GFP-expressing cells (Trizol, Sigma). Samples for each group in triplicate were processed for Illumina bead arrays (Illumina HT-12) by the MSKCC genomics core facility according to the specifications of the manufacturer.

2013-12-31 | E-GEOD-46098 | biostudies-arrayexpress

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