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Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [bulk RNA-seq]

ABSTRACT: Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [bulk RNA-seq]

PROVIDER: PRJNA610609 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11245662_1.fastq.gz	Fastqsanger.gz
	SRR11245662_2.fastq.gz	Fastqsanger.gz
	SRR11245663_1.fastq.gz	Fastqsanger.gz
	SRR11245663_2.fastq.gz	Fastqsanger.gz
	SRR11245664_1.fastq.gz	Fastqsanger.gz

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Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex

Project description:Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex

| PRJNA610604 | ENA

Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [single-cell RNA-seq]

Project description:Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [single-cell RNA-seq]

| PRJNA610608 | ENA

Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [bulk RNA-seq]

Project description:Purpose: To gain futher insight into how STING regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E13 STING conditional knock out mice and littermate wild-type. Methods: Total RNA from E13 telencephalic tissue of wild-type(WT) and STINGf/f;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and STINGf/f;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the down or up-regulated genes showed obvious enrichment of biological processes related to brain development and cell fate commitment. These results reflected STING plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how STING gene contribute to brain cortical development.

2020-03-06 | GSE146455 | GEO

Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [single-cell RNA-seq]

Project description:Purpose: To gain futher insight into how STING causes abnormal cortical development in mice ,single cell RNA-seq was used to analyze the cell type changes resulting from the cerebral cortices of P0 STING conditional knock out mice and littermate wild-type. Methods: Single cell isolation was prepared from P0 telencephalic tissue of wild-type(WT) and STINGf/f;Nestin-Cre mice. The fragmented cDNAs containing barcode and UMI sequences was built the library . Agilent 2100 Bioanalyze was used to quality controlled and quantified.Single cell RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Clustering and labeling of these cells visualized on a t-SNE plot between the wild-type(WT) and STINGf/f;Nestin-Cre mice brain cortex Conclusions: Single cell RNA-seq data would provide a overall understanding of how STING gene influences cortical development in mice.

2020-03-06 | GSE146456 | GEO

Deficiency of STING Signaling in Embryonic Cerebral Cortex Leads to Neurogenic Abnormalities and Autistic-Like Behaviors.

Project description:STING is known as a central adaptor for sensing cytosolic DNA sensing. Recent studies have provided evidence that STING response is divergent among different cell types. Here, this work demonstrates that STING controls neural progenitor cells (NPCs) by sensing DNA damage in NPCs. The deletion of STING reduces neuronal differentiation and increases proliferation of mouse and human NPCs. Furthermore, STINGcKO mice display autistic-like behaviors. In NPCs, STING specifically recruits IKK? and activates nuclear factor ?B (NF-?B) through phosphorylation. NF-?B binds to ALX4 promoter and triggers ALX4 transcription. In addition, tumor necrosis factor ?, an activator of NF-?B, can rescue some phenotypes caused by STING deletion in mice. Together, the findings show that STING signaling is essential for neuronal gene expression program and has profound consequences on brain function.

| S-EPMC7710002 | biostudies-literature

Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex

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

2020-03-06 | GSE146457 | GEO

Loss of histone methyltransferase ASH1L in the developing mouse brain causes autistic-like behaviors

Project description:Autism spectrum disorder (ASD) is a neurodevelopmental disease associated with various gene mutations. Recent genetic and clinical studies report that mutations of the epigenetic gene ASH1L are highly associated with human ASD and intellectual disability (ID). However, the causality and underlying molecular mechanisms linking ASH1L mutations to genesis of ASD/ID remains undetermined. Here we show loss of ASH1L in the developing mouse brain is sufficient to cause multiple developmental defects, core autistic-like behaviors, and impaired cognitive memory. Gene expression analyses uncover critical roles of ASH1L in regulating gene expression during neural cell development. Thus, our study establishes a new ASD/ID mouse model revealing the critical function of an epigenetic factor ASH1L in normal brain development, a causality between Ash1L mutations and ASD/ID-like behaviors in mice, and potential molecular mechanisms linking Ash1L mutations to brain functional abnormalities.

2021-05-23 | GSE173262 | GEO

Setd5 haploinsufficiency alters neuronal network connectivity and leads to autistic-like behaviors in mice

Project description:Setd5 haploinsufficiency alters neuronal network connectivity and leads to autistic-like behaviors in mice

| PRJNA495634 | ENA

Loss of histone methyltransferase ASH1L in the developing mouse brain causes autistic-like behaviors

Project description:Loss of histone methyltransferase ASH1L in the developing mouse brain causes autistic-like behaviors

| PRJNA724987 | ENA

The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

Project description:The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

| PRJNA1110187 | ENA