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Loss of Cic leads to aberrant neural stem cell proliferation and differentiation and promotes gliomagenesis

ABSTRACT: Mouse neural stem cells were generated from conditional knockout mice (Cicflox/flox) or the wild trype control mice (Cic+/+). Cic is conditionally knocked out following expression of Cre-recombinase. Cre-recombinase was incorporated in vitro via adenoviral-Cre transduction.

ORGANISM(S): Mus musculus

PROVIDER: GSE95012 | GEO | 2018/02/13

REPOSITORIES: GEO

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Effects of IDH1-R132H on mouse neural stem cells

Project description:Mouse neural stem cells were generated from conditional knock-in mice. Mutant IDH1 is conditionally expressed following expression of Cre-recombinase. Cre-recombinase was incorporated in vitro via adenoviral-Cre recombinase. Addtionally, adenoviral-GFP was also used to control for effects of adenoviral infection. D-2HG, the metabolic product of IDH1-R132H, was detected in cell lines post-cre transduction

2017-08-22 | GSE88828 | GEO

The role of CIC in brain development and neuronal differentiation (RNA-Seq)

Project description:RNA_seq analysis for Nes Cre;CIC+/+ vs.Nes Cre;CICflox/flox mouse brain

2020-04-15 | GSE131299 | GEO

Expression of the CIC-DUX4 fusion oncoprotein mirrors human CIC-rearranged sarcoma in a transgenic mouse model (ChIP-Seq)

Project description:CIC-DUX4 sarcoma (CDS) is a rare but highly aggressive undifferentiated small round cell sarcoma driven by a fusion between the tumor suppressor Capicua (CIC) and DUX4. Currently, there are no effective treatments and efforts to identify and translate better therapies is limited by the scarcity of tissues and patients. To minimize, we made three genetically engineered mouse models of CDS (Ch7CDS, Ai9CDS, and TOPCDS). Remarkably, chimeric mice from all three models developed spontaneous tumors and widespread metastasis in the absence of Cre-recombinase. The penetrance of spontaneous (Cre-independent) tumor formation was complete irrespective of bi-allelic CIC function and loxP site proximity. Characterization of primary and metastatic mouse tumors showed that they consistently expressed the CIC-DUX4 fusion protein as well as other downstream markers of the disease authenticating them as CDS. Lastly, tumor-derived cell lines were generated and ChIP-seq was preformed to map fusion-gene specific binding using an N-terminal HA epitope tag. These datasets, along with paired H3K27ac ChIP-seq maps, validate CIC-DUX4 as a neomorphic transcriptional activator and point to ETS family transcription factors as cooperative and redundant drivers of the core regulatory circuitry.

2023-10-19 | GSE241370 | GEO

Expression of the CIC-DUX4 fusion oncoprotein mirrors human CIC-rearranged sarcoma in a transgenic mouse model (RNA-Seq)

2023-10-19 | GSE241369 | GEO

Disruption of the ATXN1-CIC complex reveals the role of additional nuclear ATXN1 interactors in spinocerebellar ataxia type 1 [CUT&RUN]

Project description:Genome wide binding profiles of CIC and H3K27ac in CIC KO (Engrailed1-Cre;Cicfl/fl), wildtype, Atxn1_154Q/2Q (SCA1), and Atxn1_154Q[V5591A;S602D]/2Q (154Q AXH) in the cerebellum

2022-12-13 | GSE218301 | GEO

BCR repertoire analysis of wild-type and Cic-null B-1a cells

Project description:Purpose: B-1a cells have a distinct BCR repertoire compared with that of B-2 cells. To examine whether CIC loss affects the BCR repertoire in B-1a cells, we analyzed mRNA sequences of immunoglobulin heavy (Igh) and light (Igk and Igl) chain genes in B-1a cells from 12-week-old control and Cicf/f;Cd19-Cre mice. Methods: Peritoneal cavity B-1a cells (IgM+, CD19+, CD5+, CD43+) were sorted by a MoFlo-XDP (Beckman Coulter). Total RNA was extracted using TRIzol Reagent (GeneAll), according to the manufacturer’s instructions. Long Read iR-Profile Reagent System (iRepertoire) was used to generate NGS libraries covering BCR chains including Igh, Igk, and Igl. Briefly, nested inside and outside primers selectively amplified all V- and C- regions and incorporated communal adaptors. Following clean up, only target amplicons, which contain 5’ and 3’ communal adaptors, were exponentially amplified. Amplified libraries were multiplexed for sequencing on the Illumina Miseq platform. Sequence reads were de-multiplexed according to the barcode sequences. Results: Trimmed reads were mapped to germline V, D and J reference sequences downloaded from the IMGT database. IgH diversity and the usage of variable (V) segments in heavy (Ighv) chain and light (Igkv and Iglv) chain genes were comparable between control and Cic-null B-1a cells. Analysis of non-templated (N)-nucleotide addition at V(D)J junctions revealed that Cic-null B-1a cells have a higher proportion of zero to two N-nucleotides-containing-BCRs than control cells. Conclusions: Our study presents the first comparative BCR repertoire analysis of wild-type and Cic-null B-1a cells. We concluded that CIC deficiency does not dramatically alter the BCR repertoire in B-1a cells.

2021-12-16 | GSE164147 | GEO

The proteomic study on kidney-specific Tmod1 knockout mice

Project description:We performed proteomic analyses on the kidneys of Tmod1 flox/flox/Ksp-Cre- (TF) and Tmod1 flox/flox/Ksp-Cre+ (TFK) mice.

2019-06-10 | MSV000083953 | MassIVE

Quantitative proteomic analysis of the livers from 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice.

Project description:We have previously shown that the HyD-LIR-Venus probe can specifically inhibit selective autophagy by suppressing the interaction of LIR-containing selective autophagy substrates and receptors with ATG8-family proteins in vivo. We generated hepatocyte-specific HyD-LIR-Venus-expressing mice (HyD-LIRflox/flox; Alb-Cre) by crossing HyD-LIRflox/flox mice, in which HyD-LIR-Venus is expressed under CAG promoter in a Cre-recombinase-dependent manner, with Alb-Cre transgenic mice that express Cre under the control of the Albumin promoter. We performed quantitative proteomic analysis of the livers of 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice using the RTS-SPS-MS3 method on Tribrid mass spectrometry.

2023-04-24 | PXD037013 | JPOST Repository

Comparison of gene expression signatures between Cre- KTC organoid organoid and Cre+ KTC organoid

Project description:To identify downstream genes involved in cholangiocarcinoma development by genetic manipulations of Kras, TGFbR2, and CDH1, we cultured the biliary organoid from the extrahepatic bile duct of Cre-negative LSL-KrasG12D;Tgfbr2flox/flox;CDH1flox/flox (KTC) mice, and induced gene recombination using a lentivirus expressing Cre-recombinase (Cre+ KTC organoid) or control lentivirus (Cre- KTC organoid). Then, we compared gene expression signatures between Cre- KTC organoid organoid and Cre+ KTC organoid.

2017-04-30 | GSE88900 | GEO

Multi-omic analyses reveal interaction networks linking CIC to cell cycle regulation

Project description:CIC encodes a transcriptional repressor inactivated by loss-of-function mutations in several cancer types, indicating that it may function as a tumor suppressor. Recent data indicate that CIC may regulate cell cycle genes in humans; however, a thorough investigation of this proposed role has not yet been reported. Here, we used single-cell RNA sequencing technology to provide evidence that inactivation of CIC in human cell lines resulted in transcriptional dysregulation of genes involved in cell cycle control. We also mapped CIC’s protein-protein and genetic interaction networks, identifying interactions between CIC and members of the Switch/Sucrose Non-Fermenting (SWI/SNF) complex, as well as novel candidate interactions between CIC and cell cycle regulators. We further showed that CIC loss was associated with an increased frequency of mitotic defects in human cell lines and a mouse model. Overall, our study positions CIC as a cell cycle regulator and indicates that CIC loss can lead to mitotic errors, consistent with CIC’s emerging role as a tumor suppressor of relevance in several cancer contexts.

2023-06-30 | PXD030942 | Pride

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