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Inhibitory input directs astrocyte morphogenesis through glial GABABR [bulk RNA-Seq]

ABSTRACT: The goal of the study is to profile (1) molecular signature of astrocytes in different developmental stages across different brain regions, (2) differential gene expression between Gabbr1 control and Gabbr1 cKO animals.

ORGANISM(S): Mus musculus

PROVIDER: GSE198632 | GEO | 2022/03/16

REPOSITORIES: GEO

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Inhibitory input directs astrocyte morphogenesis through glial GABABR [scRNA-Seq]

Project description:The goal of the study is to profile molecular signature of different cell populations between Gabbr1 control and Gabbr1 cKO animals.

2022-03-16 | GSE198357 | GEO

Inhibitory input directs astrocyte morphogenesis through glial GABABR

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

2022-03-16 | GSE198633 | GEO

Inhibitory input directs astrocyte morphogenesis through glial GABA<sub>B</sub>R.

Project description:Communication between neurons and glia has an important role in establishing and maintaining higher-order brain function1. Astrocytes are endowed with complex morphologies, placing their peripheral processes in close proximity to neuronal synapses and directly contributing to their regulation of brain circuits2-4. Recent studies have shown that excitatory neuronal activity promotes oligodendrocyte differentiation5-7; whether inhibitory neurotransmission regulates astrocyte morphogenesis during development is unclear. Here we show that inhibitory neuron activity is necessary and sufficient for astrocyte morphogenesis. We found that input from inhibitory neurons functions through astrocytic GABAB receptor (GABABR) and that its deletion in astrocytes results in a loss of morphological complexity across a host of brain regions and disruption of circuit function. Expression of GABABR in developing astrocytes is regulated in a region-specific manner by SOX9 or NFIA and deletion of these transcription factors results in region-specific defects in astrocyte morphogenesis, which is conferred by interactions with transcription factors exhibiting region-restricted patterns of expression. Together, our studies identify input from inhibitory neurons and astrocytic GABABR as universal regulators of morphogenesis, while further revealing a combinatorial code of region-specific transcriptional dependencies for astrocyte development that is intertwined with activity-dependent processes.

| S-EPMC10733939 | biostudies-literature

Inhibitory input directs astrocyte morphogenesis through glial GABABR

Project description:Inhibitory input directs astrocyte morphogenesis through glial GABABR

| PRJNA816188 | ENA

Inhibitory input directs astrocyte morphogenesis through glial GABABR [scRNA-Seq]

Project description:Inhibitory input directs astrocyte morphogenesis through glial GABABR [scRNA-Seq]

| PRJNA814686 | ENA

Inhibitory input directs astrocyte morphogenesis through glial GABABR [bulk RNA-Seq]

Project description:Inhibitory input directs astrocyte morphogenesis through glial GABABR [bulk RNA-Seq]

| PRJNA816191 | ENA

Astrocyte growth during morphogenesis is driven by the Tre1/S1pr1 phospholipid-binding G protein-coupled receptor

Project description:TRAPseq was performed on Drosophila melanogaster astrocytes at different stages of development to assess the changes in gene translation that occur in astrocytes at these different stages.

2023-09-25 | GSE242729 | GEO

In vivo analysis of astrocyte ribosome-associated mRNA after traumatic spinal cord injury

Project description:Analysis of gene expression by astrocytes or non-astrocyte cells in spinal cord injury (SCI) lesions may lead to the identification of molecules that impact on axon regrowth. We conducted genome-wide RNA sequencing of (i) immunoprecipitated astrocyte-specific ribosome-associated RNA (ramRNA) from WT or STAT3-CKO astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples 14 days following SCI. DOI: 10.1038/nature17623 Young adult female mGFAP-Cre-RiboTag or mGFAP-Cre-RiboTag-STAT3-LoxP mice underwent severe crush SCI at thoracic level 10. 14 days following SCI, the central 3mm of the SCI lesion was extracted, homogenized and (i) astrocyte-specific ribosome-associated RNA (ramRNA) precipitated via a hemagglutinin (HA) tag targeted to either WT (n=4) or STAT3-CKO (n=3) astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples. Sex and age-matched mGFAP-Cre-RiboTag mice served as uninjured controls (n=4).

2016-03-30 | E-GEOD-76097 | biostudies-arrayexpress

Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

Project description:Astrocytes are intimately linked with brain blood vessels, a relationship critical for neuronal function. However, astroglial factors driving these physical and functional associations during postnatal brain development have yet to be identified. By characterizing structural and transcriptional changes in mouse cortical astrocytes during the first two postnatal weeks, we find that high-mobility group box 1 (Hmgb1), normally upregulated with injury and involved in adult cerebrovascular repair, is highly expressed in astrocytes at birth and then decreases rapidly. Astrocyte-selective ablation of Hmgb1 at birth affects astrocyte morphology and endfoot placement, alters distribution of endfoot proteins connexin43 and aquaporin-4, induces transcriptional changes in astrocytes related to cytoskeleton remodeling, and profoundly disrupts endothelial ultrastructure. While lack of astroglial Hmgb1 does not affect the blood-brain barrier or angiogenesis postnatally, it impairs neurovascular coupling and behavior in adult mice. These findings identify astroglial Hmgb1 as a key player in postnatal gliovascular maturation.

2023-07-10 | GSE236429 | GEO

Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

Project description:Astrocytes are intimately linked with brain vessels, a relationship that is critical for neuronal health and function. However, key astroglial molecular factors that drive these physical and functional associations during postnatal brain development have not yet been identified. We characterized structural and transcriptional changes in mouse cortical astrocytes and microvessels during the first two postnatal weeks and found that high-mobility group box 1 (Hmgb1), normally upregulated with injury and involved in adult cerebrovascular repair, was highly expressed in astrocytes at birth to then decreased rapidly. Astrocyte-selective ablation of Hmgb1 in newborn mice affected astrocyte morphology and endfoot placement, induced disruption of endfoot proteins connexin43 and aquaporin-4, induced transcriptional changes in astrocytes, and profoundly altered endothelial cell ultrastructure. While lack of astroglial Hmgb1 did not affect the blood-brain barrier or angiogenesis postnatally, it impaired neurovascular coupling and behavior in adult mice. These findings identify astroglial Hmgb1 as a key player in postnatal gliovascular maturation.

2023-06-13 | GSE224784 | GEO

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