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Cx3Cr1-Cre induction leads to microglial activation and IFN-1 signaling caused by DNA-damage in early postnatal brain

ABSTRACT: Cx3Cr1-Cre induction leads to microglial activation and IFN-1 signaling caused by DNA-damage in early postnatal brain

PROVIDER: PRJNA786338 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17134513.fastq.gz	Fastqsanger.gz
	SRR17134514.fastq.gz	Fastqsanger.gz
	SRR17134515.fastq.gz	Fastqsanger.gz
	SRR17134516.fastq.gz	Fastqsanger.gz

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Cx3Cr1-Cre induction leads to microglial activation and IFN-1 signaling caused by DNA-damage in early postnatal brain

Project description:Cx3cr1CreER driven Cre-recombinase (Cre) is a widely used genetic tool for enabling gene manipulation in microglia and macrophages. However, an in-depth analysis for the possible detrimental effects of Cre-activity in microglia, surprisingly remains missing. Here we demonstrate an age-dependent sensitivity of microglia to Cx3cr1-Cre-toxicity, wherein Cre-induction specifically in early postnatal microglia is detrimental for microglial development, proliferation and function. Tamoxifen (TAM) induced Cre-activity leads to microglial activation, type1-interferon (IFN-1) signaling and increased phagocytosis, causing aberrant synaptic pruning during early postnatal period and anxiety behavior in later age. The detrimental effects of Cre-induction are caused due to DNA-damage induced toxicity in microglia, and is limited to the early postnatal period, showing no detrimental effects in adult microglia. Thus, our study reveals the age-dependent vulnerability of microglia to Cre-activity, thereby highlighting age-dependencies of Cre-action, which could be especially applicable in the broader context of environment-responsive cell-types.

2021-12-08 | GSE190207 | GEO

Investigation of cerebrum proteomic changes in CX3CR1 deficient middle aged mouse

Project description:The aging brain shows changes in microglial function, morphology, and phenotype, indicating chronic microglial activation. CX3CR1 is crucial for microglial chemotaxis, phagocytosis, and activation. However, its exact role in the aging brain is not well understood. In this study, we examined the expression of CX3CR1 in the brains of middle-aged mice (10 months old) and explored its functional implications by conducting proteomic profiling in CX3CR1-deficient mouse cerebrum. Proteomic analysis revealed an enrichment of differentially expressed proteins (DE-proteins) in the cerebrum of middle-aged mice in GO pathways such as “synapse”, “translation”, and “ribosome”. CX3CR1 deficiency affected protein levels in GO pathways such as “glutamatergic synapse” and “RNA splicing.” We also detected the proteomics in age-matched 5xFAD mice for comparison, since this mouse strain featured aberrant microglial activation and CX3CR1 upregulation in the hippocampus and frontal cortex. Our findings demonstrated that CX3CR1 was upregulated to maintain synaptic homeostasis probably through regulating microglial activation and phagocytosis in the brains of middle-aged mice. CX3CR1 may represent a promising therapeutic target for alleviating the effects of aging and preventing neurodegeneration.

2025-07-05 | PXD058961 | Pride

Differential expression analyses in microglial cells from APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice treated with tamoxifen vs APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice non treated

Project description:Differential expression analyses in microglial cells from APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice treated with tamoxifen vs APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice non treated

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Single-cell transcriptomics of spinal microglia from Cx3cr1-Cre-YFP x flxRunx1 mice

Project description:Runx1 is a transcription factor known to be involved in microglial reactivity in the perinatal period, but its role in regulating microglia reactivity later in life is not well understood. Transgenic mice with a conditional inducible deletion of the transcription factor Runx1 in Cx3cr1 positive cells were generated to further investigate. Immunohistochemical labelling and electron microscopy, flow cytometry and quantitative PCR showed indications of altered microglial phenotype in knock-out mice. Single-cell seq was pursused to further delineate the microglial populations in wild-type and Runx1 knock-out mice.

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:CX3CR1, one of the highest expressed genes in microglia in mice and humans, is implicated in numerous microglial functions. However, the molecular mechanisms underlying Cx3cr1 signaling are not well understood. Here, we analyzed transcriptomes of Cx3cr1-deficient microglia under varying conditions by RNA-Seq. In 2 mos mice, Cx3cr1 deletion resulted in the downregulation of a subset of immune-related genes, without substantial epigenetic changes in markers of active chromatin. Surprisingly, Cx3cr1-deficient microglia from young mice exhibited a transcriptome consistent with that of aged Cx3cr1-sufficient animals, suggesting a premature aging transcriptomic signature. Immunohistochemical analysis of microglia in young and aged mice revealed that loss of Cx3cr1 modulates microglial morphology in a compatible fashion. Our results suggest that CX3CR1 may regulate microglial function in part by modulating the expression levels of a subset of inflammatory genes during chronological aging, making Cx3cr1-deficient mice useful for studying aged microglia.

2019-10-01 | GSE130960 | GEO

A comparative analysis of microglial inducible Cre lines

Project description:We investigated the effects of tamoxifen, CreER recombination, and genetic manipulations to genes whose promoters are used to driving CreER expression on microglial gene expression across 4 different microglial inducible Cre lines.

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A comparative analysis of microglial inducible Cre lines

Project description:A comparative analysis of microglial inducible Cre lines

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

2019-11-25 | GSE131869 | GEO

Microglia RNAseq from ARID1A fl/fl cx3cr1-cre mouse line

Project description:Microglia RNAseq from ARID1A fl/fl cx3cr1-cre mouse line Raw sequence reads

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Human induced pluripotent stem cell-derived microglia with a CX3CR1-V249I genetic variant exhibit dysfunctional phenotypes and modulate neuronal growth and function

Project description:The involvement of microglia in neurodegenerative diseases has drawn increasing attention, as many genetic risk factors are preferentially expressed in microglia. Microglial fractalkine receptor (CX3CR1) signaling regulates many key microglial functions, and the CX3CR1-V249I single nucleotide polymorphism (SNP) has been associated with increased risk for multiple neurodegenerative conditions, including Alzheimer’s disease, yet its functional consequences in human microglia remain unexplored. In this study, we generated iPSC-derived human microglia-like cells (hMGLs) and found that the CX3CR1-V249I variant increased susceptibility to starvation-induced cell death, reduced amyloid-beta uptake, altered microglial morphology, and impaired migration, with more pronounced effects in homozygous cells. Co-culture with neurons demonstrated that hMGLs with the CX3CR1-V249I variant misregulated neuronal properties, including abnormal neuronal growth as well as an induction of neuronal hyperexcitability. These findings highlight the critical role of CX3CR1 in regulating microglial function and implicate the V249I variant in driving pathogenic microglial states relevant to neurodegeneration.

2025-07-23 | GSE302806 | GEO

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