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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

ABSTRACT: Microglial cells were isolated by flow citometry using specific markers (CD45+/ CD11b+) and their global gene expression profile was analyzed. This data were used to study the role of HIF1A in microglia associated to Aβ plaques. In this dataset, we include the expression data obtained in microglial cells from a model of gain of function of HIF1A in APP-PSEN1/+ mice. (18 moth-old-age) mice model using a specific marker for this cell type (CD31+). Functional enrichment analyses were carried out through GSEA, where we have included specific categories potentially involved with blood vessel formation.

ORGANISM(S): Mus musculus

PROVIDER: GSE168059 | GEO | 2021/03/08

REPOSITORIES: GEO

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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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The quantitative analysis of transcriptomes derived from MLL-AF10 flox cells and MLL-AF10 (Tip60 flox/flox, Cre-ERT2) cells with or without the treatment of 4-OHT

Project description:Chromosome translocations involving the MLL gene are common rearrangements in leukemia. Such translocations fuse the MLL 5’-region in frame to partner genes , and the resultant fusion proteins can cause MLL-related leukemia. MLL-fusions activate transcription of target genes such as the HoxA cluster and Meis1, but the underlying mechanisms remain elusive. We found that the MLL-AF10 fusion recruits Tip60 to the Hoxa9 locus, where it acetylates H2A.Z, thereby promoting Hoxa9 expression. Following conditional deletion of Tip60, hypoacetylation of H2A.Z was accompanied by recruitment of Ezh2, the catalytic subunit of PRC2, suggesting that nucleosomes with hypoacetylated H2A.Z are the preferential targets of Ezh2. Our findings suggest that MLL-AF10 achieves active chromatin states by recruiting Tip60, which acetylates H2A.Z to prevent gene silencing by Ezh2.

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Adiponectin-cre FTO flox/flox and FTO flox/flox mouse white fat tissues

Project description:Single nucleotide polymorphisms in intron 1 of the fat mass and obesity-associated (FTO) gene were found to be associated with an increased risk of adult obesity. Enhanced FTO expression in mice leads to hyperphagia, increased fat mass, and higher body weight. Neuronal-specific FTOâ??deleted mice have an identical lean body weight phenotype to global FTO-deleted mice. The physiological role of adipose FTO in the homeostasis of energy regulation remains to be elucidated. We used microarrays to elucidate the metabolic pathways that are regulated by FTO in the white fat. FTO flox/flox and Adiponectin-cre FTO flox/flox (AFO) mice were fed with chow diet. White fat tissues from epididymal adipose pad were harvested under ad lib condition for RNA isolation. Three independent pools of FTO flox/flox and AFO mouse white fat RNA were included in the study.

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Gene expression profile of Dnmt1 flox/flox, Dnmt3a flox/flox, Dnmt3b flox/flox, cre negative (Wild type) and Dnmt1 flox/flox, Dnmt3a flox/flox, Dnmt3b flox/flox, Rx-cre (Triple mutant) murine retina transcriptomes

Project description:Purpose: The goal of this study was to identify the gene expression profile of mouse retina which carries deletions in Dnmt1, Dnmt3a and Dnmt3b genes. Method: Retinal mRNA profiles of Postnatal day 15 wild type mice and Dnmt1, Dnmt3a and Dnmt3b mutant mice were generated by deep-sequencing

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Next Generation Sequencing analysis of Hes1+/+ Cre-ERT2 and Hes1fl/fl Cre-ERT2 bone marrow derived macrophages transcriptomes.

Project description:To evaluate the potential role of Hes1 in regulation of type I IFNs and the downstream ISGs expression, we generated the bone marrow-derived macrophages (BMDMs) from Hes1+/+ Cre-ERT2 and Hes1fl/fl Cre-ERT2 mice. RNA-sequencing analysis of Poly(I:C) [(polyinosinic: polycytidylic acid), a mimic of viral double-stranded RNA]-treated BMDMs revealed that 49 genes were induced more than two-fold by Poly(I:C) for 3 hrs in Hes1-deficient BMDMs relative to their expression in Hes1+/+Cre-ERT2 cells. Notably, 67.3% of these upregulated genes were ISGs by screening the Interferome database, suggesting that Hes1 inhibits expression of TLR-mediated ISGs,these results indicated that Hes1 negatively regulates TLR3-mediated induction of ISGs in macrophages.

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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

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