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RNA-seq of mouse glioma tumors with or without ASCL1

ABSTRACT: Tamoxifen was administered to Glast-CreER;Nf1-flox/flox;Tp53-flox/flox or Glast-CreER;Ascl1-flox/flox;Nf1-flox/flox;Tp53-flox/flox at E14.5 to induce tumors in the brain

ORGANISM(S): Mus musculus

PROVIDER: GSE152400 | GEO | 2020/11/05

REPOSITORIES: GEO

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Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic

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

Gene expression changes in Apc-mutant mouse intestinal organoids with and without deleting the Prox1 transcription factor

Project description:We isolated and selected intestinal adenoma organoids from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox mice and added tamoxifen to induce the deletion of the Apc and Prox1 genes in the intestinal epitheliul ex vivo. Microarray experiments were carried out 7 days after the addition of tamoxifen. Total RNA obtained from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox organoids were compared 7 days after the addition of tamoxifen and 5 days after the selection for Apc-mutant organoids in the absence of the Wnt-agonist R-Spondin1.

2014-08-15 | E-GEOD-47568 | biostudies-arrayexpress

Low-grade glioma microglia

Project description:To examine the effect of Nf1 inactivation in astrocytes on normal microglia in the optic nerve, microglia from Nf1 flox/flox (FF) and Nf1 flox/flox; GFAP-Cre (FFC) were flow sorted. High throughput RNA-seq was employed to compare the expression profiles, and upregulated genes in microglia supportive to Nf1 deficient astrocytes were verified.

2020-07-03 | GSE65865 | GEO

Gene expression changes in Apc-mutant mouse intestinal organoids with and without deleting the Prox1 transcription factor

2014-08-15 | GSE47568 | GEO

Impact of IRP deficiency on the proteome of Ly6G+ cells from the bone marrow in mice

Project description:The overall objective of the project is to evaluate the effects of loss of function of iron regulatory proteins (IRP1, encoded by Aco1)-1 and -2 (IRP2, encoded by Ireb2) during adult life. Mice carrying floxed Aco1 and Ireb2 alleles were crossed to a knockin strain expressing a tamoxifen-inducible CRE recombinase under the control of the Rosa26 promoter. The resulting Aco1flox/flox,Ireb2flox/flox,Rosa26+/CreERT2 mice are designated P1/2-KO; littermates lacking the CreER sequence (Aco1flox/flox,Ireb2flox/flox,Rosa26+/+) serve as reference and are designated P1/2-CTR. Adult mice were injected (i.p.) with tamoxifen on day 1 and day 3 to ablate the IRPs in the whole body, and were sacrificed on day 10 for analysis. Bone marrow cells were collected and LY6G+ cells were magnetically sorted for proteome analysis by LC-MS/MS using an Ultimate 3000 UPLC system connected to an Orbitrap Exploris 480 mass spectrometer.

2023-03-11 | PXD032077 | Pride

Gene expression changes in Apc-mutant mouse intestinal organoids 7 and 20 days after the induction of the Apc deletion

Project description:We isolated and selected intestinal adenoma organoids from Lgr5-EGFP-IRES-CreER; Apcflox/flox mice and added tamoxifen to induce the deletion of the Apc gene in the intestinal stem cells. Gene expressions on day7 and day20 after the addition of tamoxifen were compared, representing two stages with different colorectal cancer stem cell content. Total RNA obtained from Lgr5-EGFP-IRES-CreER; Apcflox/flox organoids were compared 7 days and 20 days after the addition of tamoxifen, cultured without the Wnt-agonist R-Spondin1.

2015-12-31 | E-GEOD-47569 | biostudies-arrayexpress

Expression analysis of MADM based glioma mouse model

Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the expression changes of genes induced by inactivation of Tp53 and Nf1 can be a clue to clarify the mechanism of gliomagenesis. We examined the expressions of glioma in MADM mouse at post-natal 150 days (n=3) and of normal brain in Tp53 and Nf1 wild type mouse at post-natal 150 days (n=2). We used SurePrint G3 Mouse GE 8×60K array slides (G4858A, Agilent Technologies).

2017-06-30 | GSE91050 | GEO

Ascl1 ChIP-seq experiment from ventral telencephalon at E14.5 embryos.

Project description:Here we performed a ChIP-seq experiment on a sample of ventral telencephalon from E14.5 embryos. This resulted in the generation of a genome-wide map of Ascl1 binding to chromatin.

2021-07-03 | E-MTAB-9751 | biostudies-arrayexpress

Silencing of ASCL1 in U87MG glioma cells

Project description:ASCL1 is known to act as transcriptional activator of notch signaling pathway. We have found that ASCL1 is over expressed in secondary glioblastoma. In order to delineate its functional role in gliomagensis we have used gene silencing approach to identify genes differentially regulated upon ASCL1 down regulation in U87MG glioma cell line.

2017-05-22 | GSE76652 | GEO

Identification of Sox9-Regulated Pathways During the Secondary Transition Stage of Pancreas Development

Project description:Sox9 target genes were identified during the secondary transition stage of pancreas development by comparing gene expression in Sox9-ablated versus wild-type pancreata using microarray analysis. Sox9 was conditionally ablated during the secondary transition in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the tamoxifen-inducible Rosa26-CreER allele (Vooijs et al., 2001). Dams were injected with 6 mg/40 g tamoxifen in corn oil at e12.5. Pancreata were manually microdissected at e15.5. Total RNA was isolated and pooled from pancreata of e15.5 Sox9fl/fl; Rosa26-CreER (mutant) versus Rosa26-CreER (wild-type) littermates for four biological replicates.

2012-08-01 | E-GEOD-28670 | biostudies-arrayexpress

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