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Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1Tdt]

ABSTRACT: Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1Tdt]

PROVIDER: PRJNA1037699 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26757805_1.fastq.gz	Fastqsanger.gz
	SRR26757805_2.fastq.gz	Fastqsanger.gz
	SRR26757806_1.fastq.gz	Fastqsanger.gz
	SRR26757806_2.fastq.gz	Fastqsanger.gz
	SRR26757807_1.fastq.gz	Fastqsanger.gz

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Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury

Project description:Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury

| PRJNA1037481 | ENA

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1Tdt]

Project description:Microglial reactivity to injury and disease is emerging as a heterogeneous, dynamic, and crucial determinant in neurological disorders. However, the plasticity and ultimate fate of disease-associated microglia (DAM) remains largely unknown. We established a lineage tracing system, leveraging the expression dynamics of Spp1, which allows for genetic labeling of DAM-like microglia and tracking their behavior during brain injury and recovery. Fate-mapping of Spp1+ microglia in juvenile stroke revealed an irreversible state of reactive microglia that are ultimately eliminated from the injured brain. In contrast, DAM-like microglia in the neonatal context exhibit high plasticity, capable of regaining a homeostatic signature and integrating into the global microglial network after recovery. Furthermore, neonatal injury has a lasting impact on microglia, rendering them intrinsically sensitized to subsequent immune challenges. Therefore, by unraveling the fate of DAM-like microglia in various neuropathological conditions, our work highlights the exceptional plasticity and innate immune memory of neonatal microglia.

2024-01-24 | GSE247391 | GEO

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1GFP]

2024-01-24 | GSE247390 | GEO

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1GFP]

Project description:Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1GFP]

| PRJNA1037479 | ENA

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury

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

2024-01-24 | GSE247394 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of primary cultured astrocytes Transcriptomes from neonatal wild type and Spp1 KO retina and optic nerve.

Project description:Purpose: The goals of this study are to investigate differential genes expression with RNA-seq between wild type and Spp1 KO retinal and optic nerve astrocytes and then to identify the effected genes after Spp1 knockout Methods: Total RNA was extracted from cultured astrocytes isolated from either C57BL/6 wild-type or Spp1 KO neonatal mice using the RNeasy Plus Micro Kit (Qiagen; 74034). mRNA profiles were generated by deep sequencing using Illumina NovaSeq 6000. The sequence reads that passed quality filters were aligned to the mouse reference genome (GRCm38) using the STAR software package. Differential expression analysis were performed using the R package DESeq2. qPCR validation was performed using SYBR Green assays. Results: After quality control and data filtering, about 40 million raw reads per sample were obtained. We mapped sequence reads per sample to the mouse reference genome (GRCm38) and identified 35825 transcripts in astrocytes of wild type and Spp1−/− mice. A total of 3624 differentially expressed genes (DEGs) were identified between wild type and Spp1−/− astrocytes, with a fold change ≥1.5 and p value <0.05. Among DEGs, 1991 were upregulated and 1633 were downregulated in the Spp1−/− astrocytes. Hierarchical clustering heat map, pathway enrichment and analysis of DEGs were performed. Conclusions: Our RNA-seq dataset represents the differentially expressed genes in theSpp1 KO astrocytes.

2022-11-23 | GSE174522 | GEO

Characterization of Spp1-TAP and Mer2-TAP interactomes

Project description:Histone H3K4 methylation is a feature of meiotic recombination hotspots shared by many organisms including plants and mammals. Meiotic recombination is initiated by programmed double strand break (DSB) formation that in budding yeast is directed in gene promoters by histone H3K4 di/trimethylation. This histone modification is indeed recognized by Spp1, a PHD-finger containing protein that belongs to the conserved histone H3K4 methyltransferase Set1 complex. During meiosis, Spp1 binds H3K4me and recruits a DSB protein, Mer2, to promote DSB formation close to gene promoters. How Set1C and Mer2 related functions of Spp1 are connected is not clear.

2018-01-30 | PXD007590 | Pride

The admixed brushtail possum genome reveals invasion history in New Zealand and novel imprinted genes

Project description:The admixed brushtail possum genome reveals invasion history in New Zealand and novel imprinted genes

| PRJNA905667 | ENA

Targeted scRNAseq of control and SPP1 stimulated human whole blood

Project description:SPP1 stimulation of human leukocytes drives proinflammatory monocyte activation and differentiation of dysregulated CD274(PDL-1)pos neutrophil phenotype.

2022-05-02 | E-MTAB-10430 | biostudies-arrayexpress

RNA seq data of B cells from naïve, OPN knockout (Spp1-/-), ONKOSCID (SCID Spp1-/-) BALB/c mice

Project description:Marginal zone (IgM[hi] CD23[lo]MZ) and Follicular B (IgM[lo] CD23[hi]FB) cells in SCID Spp1-/- mice have different profile from naïve and Spp1-/- B cells. In addition, OPN mutation on the SCID background induced upregulation of genes involved in DNA replication and class switching of B cells

2021-08-20 | GSE118826 | GEO

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