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Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

ABSTRACT: Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

PROVIDER: PRJNA1127524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29532831_1.fastq.gz	Fastqsanger.gz
	SRR29532831_2.fastq.gz	Fastqsanger.gz
	SRR29532832_1.fastq.gz	Fastqsanger.gz
	SRR29532832_2.fastq.gz	Fastqsanger.gz

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Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

Project description:Dysregulation of epigenetic mechanisms play crucial roles in brain development and disease. Emerging evidence suggests that RACK7, an epigenetic reader protein, may play a role in brain development, but in vivo exploration of RACK7 in neural development and the underlying mechanisms are still lacking. Here, we established a conditional knock-out Rack7 mouse model and show that Rack7-deficient mice exhibit overt developmental defects. Multicomplex immunofluorescence staining (mIF) of cell-type specific markers indicates that the developmental defects are associated with compromised astrocyte development. Mechanistically, we surprisingly found RACK7 interacts with PRC2 complex, which acts as the histone H3K27 methyltransferase. Our results suggest RACK7 binding with PRC2 complex helps to establish the proper genomic location of histone H3K27me3 modification. Deletion of Rack7 in astrocyte leads to a remarkable decrease of H3K27me3 chromatin enrichment. genome-wide?. Functionally, we found RACK7 works together with H3K27me3 to prevent overactivation of Wnt signaling pathway and other astrocyte differentiation genes. Collectively, our study provides new insights into the cellular and molecular mechanisms underlying brain development regulated by RACK7.

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Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

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Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

Project description:Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

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Astrocyte, OPC, OL in rat postnatal development

Project description:Proteomic analysis of astrocyte, OPC, OL isolated from postnatal day 5 rat.

2022-05-03 | PXD033729 |

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.

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RACK7 ChIP-seq in pediatric glioblastomas cell lines.

Project description:We identified that RACK7 recognizes the histone H3.3G34R mutaion in vitro. In order to determine the interaction between RACK7 and H3.3G34R mutaion in cells, we used three pediatric glioblastoma (pGBM) cell lines. SJ-HGGx6c(R6) and SJ-HGGx42c(R42) have heterozygous G34R mutation, while SJ-HGGx39c(WT39) has wildtype H3F3A, which encodes H3.3, and we also corrected H3.3G34R in R6 and R42 cells to wildtype H3.3 by CRISPR/Cas9 mediated knock-in. Finally, we performed RACK7 ChIP-seq in these cell lines to explore the function of RACK7 and H3.3G34R mutation.

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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.

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Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

Project description:Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

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Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

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RACK7 Senses and Fine-Tunes Enhancer Activity [TT-Seq]

Project description:Enhancers regulate dynamic gene expression in a spatiotemporal specific manner. A number of positive as well as negative regulators of enhancers have been reported so far. However, whether and how these regulators sense enhancer activity dynamics remains unclear. In this study, we show that a specific enhancer regulator, RACK7, swiftly re-distributes from repressed enhancers to activated enhancers in response to a plethora of acute stimulations. We further show that this process depends on transcription and RACK7 positively regulates enhancer activation by promoting the recruitment of RNA polymerase II. Taken together, our findings suggest that RACK7 senses enhancer activity changes and facilitates their activation during acute stimulations.

2025-07-01 | GSE282268 | GEO

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