Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNA-seq of microglia from Cx3cr1CreERT2(Litt) adult mice reveals gene expression profile after TAM treatment.

ABSTRACT: The Cx3cr1CreERT2(Litt) mouse model is widely used for in-depth studies of myeloid cells, including microglia. In this study, we employed single-cell RNA sequencing (scRNA-seq) to characterize microglial responses to tamoxifen (TAM) administration in adult Cx3cr1CreERT2(Litt) mice. Our analysis revealed a prolonged TAM-dependent induction of CDKN1A in the microglial population, highlighting a effect of the Cre-induction system itself.

ORGANISM(S): Mus musculus

PROVIDER: GSE304771 | GEO | 2025/08/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of TAM treatment on gene expression profile of microglia from Cx3cr1CreERT2 mouse lines.

Project description:Microglia, the resident macrophages in the central nervous system (CNS), have been intensively studied using rodent genetic models, including the Cx3cr1-Cre mouse line. These mice have enabled the in-depth analyses of the biological features and functions of myeloid cells, including microglia. Occasionally, these Cx3cr1CreERT2 tools have yielded conflicting outcomes, the underlying mechanism of which remains unclear. Here, we comparatively characterize the two available Cx3cr1CreERT2 lines (Cx3cr1CreERT2(Litt) and Cx3cr1CreERT2(Jung)). We find a mouse line-specific and TAM-dependent persistent induction of CDKN1A in microglia of Cx3cr1CreERT2(Litt) mice, but not in those of Cx3cr1CreERT2(Jung) mice, which affects experimental readouts with altered proliferative capacity. Furthermore, aberrant cellular alterations observed in postnatal Cx3cr1CreERT2(Litt) microglia are mitigated by a functional inhibition of CDKN1A. Together, these findings underscore the significance of mouse line-specific phenomena that alter microglial outcomes in a CDKN1A-dependent manner, highlighting the importance of rigorous validation of genetic mouse tools.

2025-08-06 | GSE304770 | GEO

Reproducible specificity and efficiency of tamoxifen-mediated cre induction across ages

Project description:Temporally controlling cre recombinase through tamoxifen (TAM) induction has many advantages for biomedical research studies. While most projects use TAM induction of mice at early post-natal or adolescence (<2m.o.) ages, age-related neurodegeneration and aging studies can require experimental designs with cre induction in older mice (>12m.o.). While anecdotally reported to be problematic, there are no published comparisons of TAM mediated cre induction at young and older ages. Cx3cr1creERT2 mice for studying microglial were crossed to a floxed NuTRAP reporter to compare cre induction at young (3m.o.) and old (18m.o) ages. Specificity and efficiency microglial labeling was identical at 24m.o. in mice induced with TAM at 3m.o. or 18m.o. of age. Age-related microglial translatomic changes were nearly identical regardless of TAM induction age. While each cre and flox mouse line should be validated before use, these findings demonstrate that TAM induction of cres can be performed even into older mouse ages.

2023-12-14 | GSE241574 | GEO

Microglia use TAM receptors to detect and engulf amyloid beta plaques

Project description:Two microglial TAM receptor tyrosine kinases - Axl and Mer - have been linked to Alzheimer’s disease, but their roles in disease have not been tested experimentally. We find that in Alzheimer’s disease and its mouse models, induced expression of Axl and Mer in amyloid plaque-associated microglia is coupled to induced plaque decoration by the TAM ligand Gas6 and its co-ligand phosphatidylserine. In the APP/PS1 mouse model of Alzheimer’s disease, sIngle cell RNAseq analysis comparing wild type microglia with those with Axl and Mer deficiency reveals a similar disease state transitional program of microglia but a dampened differential expression of numerous AD siganture genes in microglia lacking TAM receptors. In line with the transcriptomic data, using two-photon microscopy, we show that genetic ablation of Axl and Mer results in microglia that are unable to normally detect, respond to, organize, or phagocytose amyloid beta plaques. These major deficits notwithstanding, and contrary to expectation, TAM-deficient APP/PS1 mice develop fewer dense-core plaques than APP/PS1 mice with normal microglia. Our findings reveal that the TAM system is an essential mediator of microglial recognition and engulfment of amyloid plaques, and that TAM-driven microglial phagocytosis does not constrain, but rather promotes, plaque development.

2021-02-25 | GSE160523 | GEO

Effect of TAM treatment on gene expression profile of microglia from Cx3cr1CreERT2 mouse lines.

Project description:Effect of TAM treatment on gene expression profile of microglia from Cx3cr1CreERT2 mouse lines.

| PRJNA1302487 | ENA

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

Characterization of the molecular signature associated with the ablation of integrin Î±6 in IECs in the Î±6ÎIEC-TAM mouse model

Project description:Transcriptome analysis of mRNAs extracted from the rectal mucosa of WT and Î±6ÎIEC-TAM mice, 15 days after tamoxifen treatment Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. We show that the specific ablation of integrin Î±6 in intestinal epithelial cells (IECs) results in spontaneous colorectal inflammation in mice. In order to characterize the earlier molecular signature involved in the onset of inflammation, we performed Affymetrix microarrays and compare control versus Î±6ÎIEC-TAM transcriptomes after tamoxifen treatment. RNAs were prepared from rectal mucosa of 3 control mice treated with tamoxifen, 4 mutant mice treated with tamoxifen and 4 mutant mice treated with NaCl. The transcriptome analysis was performed using the Affymetrix Mouse Gene 1.0 ST arrays. Images were processed using affymetrix GeneChipÂ® Command ConsoleÂ® Software (AGCC) (version 2.0) and numerical values were generated using Affymetrix Expression Consoleâ¢ Software (version 1.1).

2016-07-07 | E-GEOD-70700 | biostudies-arrayexpress

Characterization of the molecular signature associated with the ablation of integrin α6 in IECs in the α6ΔIEC-TAM mouse model

Project description:Transcriptome analysis of mRNAs extracted from the rectal mucosa of WT and α6ΔIEC-TAM mice, 15 days after tamoxifen treatment Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. We show that the specific ablation of integrin α6 in intestinal epithelial cells (IECs) results in spontaneous colorectal inflammation in mice. In order to characterize the earlier molecular signature involved in the onset of inflammation, we performed Affymetrix microarrays and compare control versus α6ΔIEC-TAM transcriptomes after tamoxifen treatment.

2016-07-07 | GSE70700 | GEO

Molecular response mechanisms of encapsulated Tamoxifen (N-TAM) on DNA damage regulatory pathways

Project description:Background: We have applied an integrative approach, including classical genomic, microarray, and refined computational systems biology to study the regulatory pathways that involve DNA damage associated with typical drug preparations of Tamoxifen (TAM). We compared the effects of newly formulated Nano-emulsions of TAM (NanoTAM or N-TAM) on cultured HTB-20 cells to those of liquid preparations of TAM. Phenotypic screening was used to identify changes induced. Implicated regulatory pathways were systematically investigated by chromatin immunoprecipitation (ChIP) and DNA microarray analyses to identify alterations in protein-DNA interactions as well as genome-wide expression patterns. While liquid solutions of clinically used TAM can have a Z-score average of thousands of nm, after encapsulation and application of high pressure particle size was ~41 nm. ChIP-chip technology was used to classify promoter regions for target genes bound by E2F4 in human primary HTB-20 cells upon treatment with TAM or N-TAM. Specific drug effects were defined by comparing results obtained for Control/Control (CC) Control/Nano (CN), TAM (Drug)/Control (TC), and N-TAM (Drug)/Nano (TN). Functional effects noted included changes in apoptosis, cell proliferation, RNA processing, DNA damage, repair and replication, lipid and protein metabolism, transport, and transcriptional regulators. Cells treated with clinical TAM only expressed the ataxia telangiectasia mutated protein ATM as well as several histone proteins important for DNA damage sensing and activation of repair proteins, while N-TAM did not illicit this response.. In contrast N-TAM could not only enter the cells it could cross the inner mitochondrial membrane, induced more apoptosis and affecting mitochondrial DNA.

2021-06-25 | GSE178880 | GEO

The effect of microglial STAT3 signaling on early postnatal brain development

Project description:Microglia play critical roles in the maturation and refinement of neural networks of the developing brain. The goal of this study was to investigate the role of microglial STAT3 in postnatal brain development. This experiment was aimed to determine gene profiles (RNA-seq) of wild-type and Stat3 mutant microglia. Cx3cr1CreERT2/+:Stat3loxP mice were generated to achieve tamoxifen-inducible deletion of exon 22 of the Stat3 gene in microglia. mRNA was prepared from acutely isolated microglia from postnatal day 8 (P8) pups that received tamoxifen from postnatal day 1 to 3. Overall, we found that Stat3 mutant produced signficantly higher levels of inlfammatory cytokines and had compromised DNA damage checkpoints.

2024-12-31 | GSE173110 | GEO

Single-cell RNA sequencing of self-maintaining lamina propria macrophages

Project description:Single-cell RNA sequencing of 697 YFP+ CD64+ lamina propria macrophages isolated from Cx3cr1CreERT2.Rosa26-LSL-YFP mice 35 weeks after tamoxifen administration

2018-07-30 | E-MTAB-6976 | biostudies-arrayexpress

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