Ontology highlight
ABSTRACT:
PROVIDER: PRJNA778933 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16885643_1.fastq.gz | Fastqsanger.gz | |||
| SRR16885643_2.fastq.gz | Fastqsanger.gz | |||
| SRR16885644_1.fastq.gz | Fastqsanger.gz | |||
| SRR16885644_2.fastq.gz | Fastqsanger.gz | |||
| SRR16885645_1.fastq.gz | Fastqsanger.gz |
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Project description:Cx3cr1CreER-Eyfp/wt mice contain a subset of microglia lacking Cre and EYFP expression. These microglial escape Cre-mediated recombination and gain a repopulation advantage following Cre-driven DTA-mediated microglial depletion.
2022-02-01 | GSE186700 | GEO
Project description:An overlooked subset of Cx3cr1wt/wt microglia in the Cx3cr1CreER-Eyfp/wt mouse has a repopulation advantage over Cx3cr1CreER-Eyfp/wt microglia following microglial depletion
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Project description:C/EBPalpha is a transcription factor critically involved in myeloid development and indispensable for formation of granulocytes. To track the cellular fate of stem and progenitor (LSK) cells, which express C/EBPalpha, we developed a mouse model expressing Cre recombinase from the Cebpa promoter and an inducible EYFP allele. We show that Cebpa/EYFP+ cells represent a significant subset of LSK cells, which predominantly give rise to myeloid cells in steady state hematopoiesis. C/EBPalpha induced a robust myeloid gene expression signature and downregulated E2A-induced regulators of early lymphoid development. In addition, Cebpa/EYFP+ cells comprise a fraction of early thymic progenitors (ETP) with robust myeloid potential. However, Cebpa/EYFP+ LSK and ETP cells retained the ability to develop into erythroid and T-lymphoid lineages, respectively. These findings support an instructive, but argue against a lineage restrictive role of C/EBPalpha in multipotent hematopoietic and thymic progenitors. We performed global gene expression profiling of double-sorted Cebpa/EYFP+ and Cebpa/EYFP- LSK cells of pooled Cebpa Cre/wt R26 EYFP reporter mice to identify differentially regulated genes in Cebpa+ versus Cebpa- LSK cells. RNA was isolated from three biological replicates of Cebpa/EYFP+ LSK cells and two biological replicates of Cebpa/EYFP- LSK cells. To determine if the identified genes were truly dependent on Cebpa expression, we also performed global gene expression profilling of Cebpa/EYFP+ and Cebpa/EYFP- fetal liver LSK cells of Cebpa Cre/fl R26 EYFP mice. Induction of Cebpa/Cre expression in these mice leads to Cre-mediated recombination of the floxed wt Cebpa allele resulting in a complete Cebpa knock-out. In this case, RNA was isolated from two biological replicates of either Cebpa/EYFP+ and Cebpa/EYFP- LSK cells. In addition, we included one biological replicate of Cebpa/EYFP+ and Cebpa/EYFP- fetal liver LSK cells of Cebpa Cre/wt R26 EYFP mice to determine the correlation of differentially regulated genes in bone marrow and fetal liver LSK cells.
2010-08-26 | E-GEOD-23800 | biostudies-arrayexpress
Project description:We previously discovered a sex-by-genotype defect in microglia function using a germline heterozygous knockout mouse model of Neurofibromatosis type 1 (Nf1+/- mice), in which only microglia from male Nf1+/- mice exhibited defects in purinergic signaling. Herein, we leveraged an unbiased proteomic approach to demonstrate that male, but not female, heterozygous Nf1+/- microglia exhibit differences in protein expression, which largely reflect pathways involved cytoskeletal organization. In keeping with potential defects in cytoskeletal function, only male Nf1+/- microglia had reduced process arborization and surveillance capacity. Next, to determine whether these microglial defects were cell autonomous or reflected adaptive responses to Nf1 heterozygosity in other cells in the brain, we generated conditional microglia Nf1-mutant knockout mice by intercrossing Nf1flox/flox with Cx3cr1-CreER mice (Nf1flox/wt; Cx3cr1-CreER mice, Nf1MG+/- mice). Surprisingly, neither male nor female Nf1MG+/- mouse microglia had impaired process arborization or surveillance capacity. In contrast, when Nf1 heterozygosity was generated in neurons, astrocytes and oligodendrocytes by intercrossing Nf1flox/flox with hGFAP-Cre mice (Nf1flox/wt; hGFAP-Cre mice, Nf1GFAP+/- mice), the microglia defects found in Nf1+/- mice were recapitulated. Collectively, these data reveal that Nf1+/- sexually dimorphic microglia abnormalities are likely not cell-intrinsic properties, but rather reflect a response to Nf1 heterozygosity in other brain cells.
2023-05-10 | PXD035881 | Pride
Project description:ER71 mutant embryos are nonviable and lack hematopoietic and endothelial lineages. To further define the functional role for ER71 in cell lineage decisions, we generated genetically modified mouse models. We engineered an ER71-EYFP transgenic mouse model by fusing the 3.9 kb ER71 promoter to the EYFP reporter gene. Using FACS and transcriptional profiling, we examined the EYFP+ populations of cells in ER71 mutant and wildtype littermates. In the absence of ER71, we observed an increase in the number of EYFP expressing cells, increased expression of the cardiac molecular program and decreased expression of the hemato-endothelial program compared to the wildtype littermate controls. We have also generated a novel ER71-Cre transgenic mouse model using the same 3.9 kb ER71 promoter. Genetic fate mapping studies revealed that the ER71 expressing cells daughter hematopoietic and endothelial lineages in the wildtype background. In the absence of ER71, these cell populations contributed to alternative mesodermal lineages including the cardiac lineage. To extend these analyses, we used an inducible ES/EB system and observed that ER71 overexpression repressed cardiogenesis. Together, these studies identify ER71 as a critical regulator of mesodermal fate decisions, acting to specify the hematopoietic and endothelial lineages at the expense of cardiac lineages. This enhances our understanding of the mechanisms that govern mesodermal fate decisions early during embryogenesis. 12samples were analyzed, including triplicates of WT; EYFP positive, WT EYFP negative, ER71 MT; EYFP positive and ER71 MT; EYFP negative cells
2011-11-02 | E-GEOD-32223 | biostudies-arrayexpress
Project description:RNA-Seq transcriptome comparison of the following cell populations (n=3-4 independent samples per cell population): a) CD11c-eYFP+ cells FACS sorted from brain of female adult mice 4 days after cerebral ischemia, b) CD11c-eYFP+ cells FACS sorted from brain of female parabiotic mice 4 days after cerebral ischemia c) CX3CR1+ microglia sorted from the ischemic brain of female CX3CR1CreERT2-ROSA26 tdTomato mice. Purpose: The goal of this study is to compare the transcriptome profile (RNA-Seq) of infiltrating cD11c-eYFP+ cells and microglia, both collected from ischemic brains of mice. Methods: RNA samples were obtained from FACS sorted eYFP+ cells of the ipsilateral brain hemisphere of CD11c-eYFP mice 4 days post-ischemia, the ipsilateral brain hemisphere of CD11c-eYFP/WT parabiotic mice 4 days post-ischemia, and from microglial cells sorted from the ipsilateral brain hemisphere of Cx3cr1CreERT2:ROSA26dTomato mice 4 days post-ischemia. NGS was performed (RNA-Seq) to compare the transcriptome of these populations. Results: the populations we compared clearly separated the differentially expressed genes in an unsupervised cluster analysis. 1509 genes were overrepresented in microglia and 1183 genes were overrepresented in CD11c-eYFP+ cells in the ischemic brain. Conclusions: Our study is the first comparative analysis of the transcriptomes of microglia and the infiltrating CD11c-eYFP+ cells derived from the ischemic brain of mice. The results show that the infiltrating CD11c-eYFP cell population in the ischemic brain tissue of parabiotic mice displays overrepresentation of genes typical of dendritic cells, immune functions, and ClassII antigen presentation, amongst others, that are not found represented in microglia.
2020-10-20 | GSE136855 | GEO
Project description:C/EBPalpha is a transcription factor critically involved in myeloid development and indispensable for formation of granulocytes. To track the cellular fate of stem and progenitor (LSK) cells, which express C/EBPalpha, we developed a mouse model expressing Cre recombinase from the Cebpa promoter and an inducible EYFP allele. We show that Cebpa/EYFP+ cells represent a significant subset of LSK cells, which predominantly give rise to myeloid cells in steady state hematopoiesis. C/EBPalpha induced a robust myeloid gene expression signature and downregulated E2A-induced regulators of early lymphoid development. In addition, Cebpa/EYFP+ cells comprise a fraction of early thymic progenitors (ETP) with robust myeloid potential. However, Cebpa/EYFP+ LSK and ETP cells retained the ability to develop into erythroid and T-lymphoid lineages, respectively. These findings support an instructive, but argue against a lineage restrictive role of C/EBPalpha in multipotent hematopoietic and thymic progenitors.
2010-08-26 | GSE23800 | GEO
Project description:Tomosyn (STXBP5) is a non-canonical SNARE protein enriched in many secretory cells and implicated in regulation of exocytosis. In neurons, loss of tomosyn affects fusion of synaptic vesicles. Here, we examined the impact of the loss of tomosyn (STXBP5) and its close paralog, tomosyn-2 (STXBP5L), on the proteome of primary mouse hippocampal neurons. To do this, we used a mouse model carrying floxed alleles of Stxbp5 and Stxbp5l genes. Primary hippocampal neurons isolated from these mice were transduced with Cre-recombinase, which expression resulted in a nearly complete loss of the two genes expression. As control, we used neurons from the same culture preparation but expressing Cre-recombinase lacking DNA-binding domain (ΔCre). This dataset provides the comparison of proteome of control ('WT') and Stxbp5/5l double knockout ('DKO') neurons.
2022-12-19 | PXD038442 | Pride
Project description:To define pericytic MyD88-dependent expression of cytokines and other immune mediators, pancreatic pericytes were isolated based on their YFP-labeling from Nkx3.2-Cre;EYFP and Nkx3.2-Cre;EYFP;MyD88 flox/flox transgenic mice.
2023-12-31 | E-MTAB-13639 | biostudies-arrayexpress
Project description:RNA-Seq transcriptome comparison of the following cell populations (n=4 independent samples per cell population): a) CD11c-eYFP+ cells FACS sorted from brain of adult mice 4 days after cerebral ischemia, b) CX3CR1+ microglia sorted from the ischemic brain of CX3CR1CreERT2-ROSA26 tdTomato mice; c) CD11c-rYFP+ cells sorted from the spleen of control mice; d) CX3CR1+ microglia sorted from the brain of control mice. Purpose: The goal of this study is to compare the transcriptome profile (RNA-Seq) of cD11c-eYFP+ cells and microglia, both collected from ischemic brains of mice, and with reference cell populations, i.e. Steady-stated microglia from brain of corresponding control mice and steady-state CD11c-eYFP cells sorted from the spleen of control mice. Methods: RNA samples were obtained from FACS sorted eYFP+ cells of the ipsilateral brain hemisphere of CD11c-eYFP mice 4 days post-ischemia, the spleen of control CD11c-eYFP mice, and from microglial cells sorted from control brain and the ipsilateral brain hemisphere 4 days post-ischemia of Cx3cr1CreERT2:ROSA26dTomato mice. NGS was perfomed (RNA-Seq) to compare the transcriptome of these populations. Results: the populations we compared clearly separated the differentially expressed genes in an unsupervised cluster analysis. 950 genes were overrepresented in microglia and 1469 genes were overrepresented in CD11c-eYFP+ cells in the ischemic brain. Conclusions: Our study is the first comparative analysis of the transcriptomes of microglia and the infiltrating CD11c-eYFP+ cells derived from the ischemic brain of mice. The results show that the infiltrating CD11c-eYFP cell population in the ischemic brain tissue of parabiotic mice displays overrepresentation of genes typical of dendritic cells, immune functions, and ClassII antigen presentation, amongst others, that are not found represented in microglia.
2020-10-20 | GSE136852 | GEO