Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lyl-1 links primitive macrophages and microglia development to neuropsychiatric disorders

ABSTRACT: Lyl-1 links primitive macrophages and microglia development to neuropsychiatric disorders

PROVIDER: PRJNA527292 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8734740.fastq.gz	Fastqsanger.gz
	SRR8734741.fastq.gz	Fastqsanger.gz
	SRR8734742.fastq.gz	Fastqsanger.gz
	SRR8734743.fastq.gz	Fastqsanger.gz
	SRR8734744.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Lyl-1 links primitive macrophages and microglia development to neuropsychiatric disorders

Project description:The regulation of developmental haematopoiesis by the bHLH transcription factor Lyl-1 has been the focus of our present study. Analysing how Lyl-1 may impact mouse developmental haematopoiesis indicated that Lyl-1 marks YS-derived primitive macrophage progenitors, as well as embryonic microglia. During ontogeny, microglia which representtissue macrophages of the central nervous system emerge from haematopoietic stem cell-independent progenitors originating from the yolk sac (YS). Activation of microglia during development is often critical and my lead to neuropsychiatric diseases in the adult. Here, we show that Lyl-1 disruption alters the development of microglia with far reaching consequences. Lyl-1-deficiency leads to decreased dendritic spine density and impaired neuronal activity, as well as impaired social interactions with increased anxiety-like behaviour. We thus identify Lyl-1 as a critical regulator of primitive macrophage and microglia development, whose disruption impacts microglia development and functionality, leading to a distinct neuropsychiatric phenotype.

2025-03-11 | GSE128378 | GEO

Targeting neural cell senescence reverses neuropsychiatric disorders

Project description:Targeting neural cell senescence reverses neuropsychiatric disorders

| PRJNA635422 | ENA

DLG2 knockout reveals neurogenic transcriptional programs underlying neuropsychiatric disorders and cognition

Project description:A complex train of events unfolds during brain development, guided by activation/repression of gene expression programs. It remains unclear how this process is disrupted in disease. Here we integrate human genetics with transcriptomic data from differentiation of human embryonic stem cells into cortical excitatory neurons. This reveals a cascade of transcriptional programs activated during early corticoneurogenesis in vitro and in vivo. Genetic variation in these programs is robustly associated with neuropsychiatric disorders and cognitive function, with variants concentrated in loss-of-function intolerant genes. Neurogenic programs also capture schizophrenia GWAS enrichment previously identified in mature excitatory neurons, suggesting that pathways activated during pre-natal development underlie disease-relevant deficits in mature neuronal function. Down-regulation of these programs in DLG2-/- lines delays expression of cell-type identity and impairs neuronal migration, morphology and action potential generation, validating predicted deficits. These data implicate specific cellular pathways underlying neurodevelopment in the aetiology of multiple neuropsychiatric disorders and cognition.

2021-11-11 | PXD029526 | Pride

DLG2 knockout reveals neurogenic transcriptional programs underlying neuropsychiatric disorders and cognition

Project description:Brain development requires a complex choreography of cell proliferation, specialisation, migration and network formation, guided by the activation and repression of gene expression programs. It remains unclear how this process is disrupted in neuropsychiatric disorders. Here we integrate human genetics with transcriptomic data from the differentiation of human embryonic stem cells into cortical excitatory neurons. This reveals a cascade of transcriptional programs, activated during early corticoneurogenesis in vitro and in vivo, in which genetic variation is robustly associated with neuropsychiatric disorders and cognitive function. Within these early neurogenic programs, genetic risk is concentrated in loss-of-function intolerant (LoFi) genes, capturing virtually all LoFi disease association. Down-regulation of these programs in DLG2 knockout lines delays expression of cell-type identity alongside marked deficits in neuronal migration, morphology and action potential generation, validating computational predictions. These data implicate specific cellular pathways and neurodevelopmental processes in the aetiology of multiple neuropsychiatric disorders and cognition.

2021-10-30 | GSE172199 | GEO

Transcriptome and chromatin accessibility landscapes across 25 human brain regions expand the susceptibility gene set for neuropsychiatric disorders [RNA-Seq]

Project description:Brain region- and cell-specific transcriptome and epigenome molecular features are associated with heritability for neuropsychiatric traits. Here, we provide an atlas of chromatin accessibility and gene expression in neuronal and non-neuronal cells across 25 distinct regions across cortical and subcortical areas of the human brain from 6 neurotypical controls. We identified extensive gene expression and chromatin accessibility differences across brain regions. We further identified variation in alternative promoter-isoform usage and enhancer-promoter interactions across brain regions and found genes with distinct promoter-isoform usage are strongly enriched for neuropsychiatric risk variants. We identified brain region-specific chromatin co-accessibility and gene-coexpression modules that are robustly associated with genetic risk variants for neuropsychiatric disorders. Using an integrative approach, we identify a novel set of genes that is enriched for neuropsychiatric disorders risk variants but is independent of cell-type specific gene expression and annotated pathways. Our results provide a valuable multi-brain region molecular regulation resource and suggest a unique contribution of epigenetic modifications from the subcortical areas to neuropsychiatric disorders.

2022-08-25 | GSE211792 | GEO

Transcriptome and chromatin accessibility landscapes across 25 human brain regions expand the susceptibility gene set for neuropsychiatric disorders [ATAC-Seq]

2022-08-25 | GSE211822 | GEO

A Novel Microglia-Specific Transcriptional Signatures Correlates with Behavioural Deficits in Neuropsychiatric Lupus (NP-SLE)

Project description:Systemic lupus erythematosus (SLE) can present with neuropsychiatric manifestations, collectively termed NP-SLE. This study identifies a microglia-specific transcriptional signature in mouse models of NP-SLE. Through RNA-seq analysis of microglia and brain-infiltrating macrophages, we uncover an 18-gene 'NP-SLE signature' and its correlation with behavioral deficits. We also observe enrichment of genes associated with disease-associated microglia (DAM), which have been implicated in neurodegenerative diseases. These findings suggest a critical role for microglia-intrinsic mechanisms in the onset of NP-SLE and provide new insights into the cellular and molecular pathways driving this disease.

2025-02-02 | GSE288261 | GEO

DLG2 knockout reveals neurogenic transcriptional programs underlying neuropsychiatric disorders and cognition

Project description:DLG2 knockout reveals neurogenic transcriptional programs underlying neuropsychiatric disorders and cognition

| PRJNA722412 | ENA

RNA Sequencing Facilitates Quantitative Analysis of Lupus (MRL/lpr) and Control（MRL/mpj）Mouse Microglia Tanscriptomes

Project description:Up to 75% of systematic lupus erythematosus (SLE) patients experience neuropsychiatric (NP) symptoms, called neuropsychiatric SLE (NPSLE), yet the underlying mechanisms remain elusive. Microglia control synaptic pruning during early postnatal brain development. The process in NPSLE remains unclear. Here, we show that microglia-coordinated elimination of synaptic terminals participated in NPSLE in MRL/lpr mice, a lupus-prone murine model. We elucidated that lupus mice developed increased depression- and anxiety-like behaviors and persistent phagocytic microglia reactivation before overt peripheral lupus pathology. Microglial engulfment of synapses explained behavioral disorders. To elucidate the mechanism of synaptic pruning by microglia, we sequenced the gene expression in sorted microglia from both lupus (MRL/lpr) mice and the wild-type (MRL/mpj) controls.

2024-03-27 | GSE201282 | GEO

Electroconvulsive Stimulation modulates Microglia. Transcriptome analysis of Biozzi-ABH mice spinal-cord microglia following electroconvulsive-seizures.

Project description:Neurostimulation by electroconvulsive therapy is highly effective in neuropsychiatric disorders by an unknown mechanism. Microglial toxicity plays a key role in chronic neuro-inflammatory brain diseases, where there is critical shortage in therapies. To investigate the direct effect of electroconvulsive seizures (ECS) on the CNS innate immune system, we performed transcriptome analysis on spinal microglia from ECS- and sham-treated naïve mice.

2022-09-01 | GSE137184 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data