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The stem cell transcription factor SOX2 is essential for astrocyte maturation and controls animal hyperactive behavior

ABSTRACT: The stem cell transcription factor SOX2 is essential for astrocyte maturation and controls animal hyperactive behavior

PROVIDER: PRJNA754275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15440589_1.fastq.gz	Fastqsanger.gz
	SRR15440589_2.fastq.gz	Fastqsanger.gz
	SRR15440590_1.fastq.gz	Fastqsanger.gz
	SRR15440590_2.fastq.gz	Fastqsanger.gz
	SRR15440591_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The stem cell transcription factor SOX2 is essential for astrocyte maturation and controls animal hyperactive behavior

Project description:Children with SOX2-deficiency develop anophthalmia/microphthalmia and display neurological impairment. Here we report an essential role for astroglial SOX2 in brain anomalies and neurological defects. Sox2-deficiency inhibited postnatal astrocyte maturation without affecting astroglial proliferation and population expansion. Mechanistically, we found that SOX2 directly bound to a cohort of astrocytic signature genes such as those involving in glutamate transport and that Sox2-deficiency remarkably reduced glutamate transporter expression and compromised astrocyte function of glutamate uptake. Behaviorally, astroglial Sox2-deficient mice developed hyperactivity in locomotion while their motor skills, social capability, and learning abilities were unaffected. We found that astroglial Sox2-deficiency results in elevated glutamatergic synapse formation and elevated excitability of striatal medium spiny neurons, which has been shown to trigger hyperactive locomotion. Our study provides new insights into the biological mechanisms underlying brain defects in children with SOX2 mutations and unveils a novel connection between astrocyte SOX2 and brain development and behavior.

2021-08-14 | GSE182032 | GEO

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior II

Project description:Astrocytes tile the central nervous system, but their functions in neural microcircuits in vivo and their roles in mammalian behavior remain incompletely defined. We used 2-photon laser scanning microscopy (2PLSM), electrophysiology, MINIscopes, RNA-seq and a new genetic approach to characterize the effects of reduced striatal astrocyte Ca2+ signaling in vivo. In wild type mice, reducing striatal astrocyte Ca2+-dependent signaling increased repetitive self-grooming behaviors by altering medium spiny neuron (MSN) activity. The mechanism involved astrocyte-mediated neuromodulation mediated by ambient GABA and was corrected by blocking astrocyte GABA transporter 3 (GAT-3). Furthermore, in a mouse model of Huntington’s disease, dysregulation of GABA and astrocyte Ca2+ signaling accompanied excessive self-grooming, which was relieved by blocking GAT-3. Assessments with RNA-seq revealed astrocyte genes and pathways regulated by Ca2+ signaling in a cell autonomous and non-cell autonomous manner, including Rab11a, a regulator of GAT-3 functional expression. Thus, striatal astrocytes contribute to neuromodulation controlling obsessive-compulsive-like behavior in mice.

2019-05-09 | GSE114756 | GEO

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior I

2019-05-09 | GSE114755 | GEO

Astrocyte-specific deletion of SOX2 promotes recovery after traumatic brain injury

Project description:Injury to the adult brain induces activation of resident astrocytes, which serves as a compensatory response modulating tissue damage and recovery. However, the mechanism governing astrocyte activation and the role of reactive astrocytes remain largely unknown. Here we show that SOX2, a transcription factor critical for stem cells and brain development, is also required for injury-induced activation of adult cortical astrocytes. Genome-wide ChIP-seq analysis reveals that SOX2 binds to regulatory regions of genes associated with signaling pathways controlling reactive gliosis, such as Socs3, Nr2e1, Notch1, and Akt2. Inducible deletion of Sox2 in adult astrocytes greatly diminishes their response to traumatic injury and, most unexpectedly, restricts injury-induced cortical loss. Together, these results uncover an essential role of SOX2 in terminally differentiated cells and implicate that SOX2-dependent reactive astrocytes may be targeted for regeneration after traumatic brain injury.

2018-02-22 | GSE85213 | GEO

Identification the Expression of Sox2 in Colorectal Cancer Tissues

Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.

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Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior

Project description:Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior

| PRJNA472565 | ENA

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior I

Project description:Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior I

| PRJNA472567 | ENA

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior II

Project description:Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior II

| PRJNA472569 | ENA

Study the epidermal regulation of mesenchymal tissue behavior using a novel rabbit animal model

Project description:In order to identify tissue specific differences in epithelial behavior following injury, we developed a novel animal model of epithelial-restricted injury in the New Zealand White rabbit. A grid of shallow incisional wounds, which extended through the entire epithelium but did not significantly damage the underlying connective tissue, were created on the skin and vaginal mucosa, and samples were taken at various times post-surgery for histology and molecular analysis. All wounds were completely re-epithelialized between 1 and 2 days post-surgery.

2010-12-01 | GSE25261 | GEO

ysblcc sox2

Project description:ysblcc sox2

| PRJEB2061 | ENA