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Mus musculus

ABSTRACT: Cerebellar granule cell replenishment postinjury by adaptive reprogramming of Nestin+ progenitors

PROVIDER: PRJNA393464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5812240_1.fastq.gz	Fastqsanger.gz
	SRR5812240_2.fastq.gz	Fastqsanger.gz
	SRR5812241_1.fastq.gz	Fastqsanger.gz
	SRR5812241_2.fastq.gz	Fastqsanger.gz
	SRR5812242_1.fastq.gz	Fastqsanger.gz

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The identification and tumorigenecity of neuronal progenitors in developing cerebellum

Project description:It is generally believed that cerebellar granule neurons originate exclusively from granule neuron precursors (GNPs) in the external germinal layer (EGL). Here we identify a rare population of neuronal progenitors in the developing cerebellum that expresses Nestin. Although Nestin is widely considered a marker for multipotent stem cells, these Nestin-expressing progenitors (NEPs) are committed to the granule neuron lineage. Unlike conventional GNPs, which reside in the outer EGL and proliferate extensively, NEPs reside in the deep part of the EGL and are quiescent. Expression profiling reveals that NEPs are distinct from GNPs, and in particular, express markedly reduced levels of genes associated with DNA repair. Consistent with this, upon aberrant activation of Sonic hedgehog (Shh) signaling, NEPs exhibit more severe genomic instability and give rise to tumors more efficiently than GNPs. These studies identify a novel progenitor for cerebellar granule neurons and a novel cell of origin for medulloblastoma. 4 samples of Nestin expressing progenitors (NEPs), 4 samples of Math1 positive cells (GNPs) and 3 samples of Neural stem cells (CD133+ NSCs) were used for microarray analysis to determine the distinct genetic profile of NEPs. 4 samples of NEP-derived tumor and 4 samples of GNP-derived tumor were used to determine the similarity of those tumors by microarray analysis.

2013-09-13 | E-GEOD-50824 | biostudies-arrayexpress

The identification and tumorigenecity of neuronal progenitors in developing cerebellum

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An increase in ROS is required for repair of the neonatal cerebellum

Project description:The neonatal mouse cerebellum shows remarkable regenerative potential upon injury at birth. Nestin-expressing progenitors (NEPs) undergo adaptive reprogramming to replenish the lost granule cell progenitors. Here, we investigate how the injury microenvironment affects NEPs’ regenerative potential and adaptive reprogramming. Single cell transcriptomic and bulk chromatin accessibility analyses of the NEPs from control and injured neonatal cerebella show a temporary increase in mechanisms involved in the response to reactive oxygen species (ROS), a known damage-associated molecular pattern. Analysis of ROS levels also confirms a temporary increase in ROS levels upon injury at postanal day 1, 1-2 days after injury, overlapping with the induction in cell death in the cerebellum. Using a transgenic mouse model that overexpresses mitochondrial catalase (mCAT) and reduces ROS levels globally, we showed that the regenerative potential of NEPs decreases upon injury to the granule cell progenitors at birth and the repair is impaired. Finally, we demonstrated that microglia are involved in adaptive reprogramming by regulating NEP migration to the external granule layer, the site of injury. Collectively, our results highlight that the changes in the tissue microenvironment such as an increase in the ROS levels are required for the adaptative reprogramming of NEPs upon injury to the granule cell progenitors at birth, highlighting the instructive roles of microenvironmental signals during regeneration in the neonatal brain.

2024-12-05 | GSE269342 | GEO

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Project description:Norrin-dependent gene expression in cerebellar granule neuron progenitors

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Project description:Gene expression of cerebellar granule cell layer

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Project description:ATAC-seq of Chd7 WT and mutant cerebellar granule neuron progenitors

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Notch signaling between cerebellar granule cell progenitors

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Cdc42 phosphorylation study - Cdc42 Regulates Neuronal Polarity during Cerebellar Axon Formation and Glial-Guided Migration

Project description:Govek et al. demonstrate conditional loss of Cdc42 in cerebellar granule cell progenitors (GCPs) perturbs GCP polarity and impairs axon patterning, glial-guided migration, and cerebellar foliation. Phospho-proteomic analysis identified polarity and cytoskeletal proteins as affected targets in Cdc42 deficient GCPs.

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WDR4 conditional knockout in mouse cerebellar granule progenitors for proteome analysis

Project description:To uncover candidates which are WDR4 downstream effectors regulating cerebellar granule neuron proliferation phenotype, we utilized quantitative proteomics analysis (TMT labeling) with granule neuron progenitors from P7 wdr4 conditional knockout (using Atoh1-Cre) and control cerebella.

2023-03-11 | PXD022319 | Pride

Transcription profiling of mouse with Hedgehog-induced medulloblastoma reveals oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors

Project description:Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors. Gene expression profiling of cerebellar tumors generated from various early and late stage CNS progenitor cells. Experiment Overall Design: Group comparisons with biological replicates

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