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Effect of osteoblast-specific constitutive activation of beta-catenin or deletion of FoxO1 on gene expression in mice

ABSTRACT: The gene expression of mice with osteoblast-specific beta-catenin activation or FoxO1 deactivation are each compared to that of Wt. A. Wt mice (n=4) B. Osteoblast specific beta-catenin constitutively expressed mice (n=3) C. Osteoblast specific FoxO1 deleted mice (n=3)

ORGANISM(S): Mus musculus

SUBMITTER: Stavroula Kousteni

PROVIDER: E-GEOD-43242 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Leukaemogenesis induced by an activating β-catenin mutation in osteoblasts.

Kode Aruna A Manavalan John S JS Mosialou Ioanna I Bhagat Govind G Rathinam Chozha V CV Luo Na N Khiabanian Hossein H Lee Albert A Murty Vundavalli V VV Friedman Richard R Brum Andrea A Park David D Galili Naomi N Mukherjee Siddhartha S Teruya-Feldstein Julie J Raza Azra A Rabadan Raul R Berman Ellin E Kousteni Stavroula S

Nature 20140115 7487

Cells of the osteoblast lineage affect the homing and the number of long-term repopulating haematopoietic stem cells, haematopoietic stem cell mobilization and lineage determination and B cell lymphopoiesis. Osteoblasts were recently implicated in pre-leukaemic conditions in mice. However, a single genetic change in osteoblasts that can induce leukaemogenesis has not been shown. Here we show that an activating mutation of β-catenin in mouse osteoblasts alters the differentiation potential of mye ...[more]

PMID: 24429522

Similar Datasets

Effect of osteoblast-specific constitutive activation of beta-catenin or deletion of FoxO1 on gene expression in mice

Project description:The gene expression of mice with osteoblast-specific beta-catenin activation or FoxO1 deactivation are each compared to that of Wt.

2014-01-21 | GSE43242 | GEO

Transcriptional Responses to beta-catenin and FoxO with and without oxidative stress

Project description:To identify novel transcriptional targets of beta-catenin and FoxO1 and FoxO3 in renal epithelial cells, we used conditionally immortalized murine proximal tubule (PT) cells (these cells, from Tgfbr2floxed mice, are described in detail in manuscript PMID: 23160515 in which Leslie Gewin is first author, JASN 2012). PT cells were either treated with Wnt3a (to activate beta-catenin) or the control diluting buffer, H2O2 to induce oxidative stress, and some were transfected with FoxO1, FoxO3, FoxO1 and 3, or scramble siRNA prior to Wnt and H2O2 treatment.

2020-06-01 | GSE144915 | GEO

β-catenin inhibits adipogenic differentiation of hypertrophic chondrocytes and promote osteogenesis

Project description:It has been shown that hypertrophic chondrocyte (HC) can become osteoblast, contributing to the formation of trabecular bone and endosteum. However, it is unclear what genes regulate the process of differentiation from chondrocyte to osteoblast. Conditional knock-out of β‑catenin in HCs can reduce the trabecular bone amount and there is also some evidence that ablation of β‑catenin in HCs can promote bone marrow adipogenesis. Conditional stabilization of β‑catenin in HCs results in osteopetrosis. In order to investigate the gene regulatory network with different dosage of β‑catenin in HC descendants (i.e. in Loss-of-Function mutant, Gain-of-Function mutant and Wildtype control), we collected HC descendant cells from proximal tibia of mice at postnatal day 5 and performed bulk RNA seq to profile the gene expression pattern in HC descendants.

2020-07-22 | GSE146111 | GEO

Mus musculus

Project description:Effect of osteoblast-specific constitutive activation of beta-catenin or deletion of FoxO1 on gene expression in mice

| PRJNA185136 | ENA

Gene expression profiles from mammary tissue of control mice, small K5M-NM-^TNM-NM-2cat hyperplasia, large K5M-NM-^TNM-NM-2cat hyperplasia and K5M-NM-^TNM-NM-2cat tumor

Project description:Basal-like breast cancer is a heterogeneous disease characterised by the expression of basal cell markers, no oestrogen or progesterone receptor expression and a lack of HER2 overexpression. Recent studies have linked activation of the Wnt/beta-catenin pathway to basal-like breast cancer. Transgenic mice expressing N-terminally truncated stabilised beta-catenin in the mammary basal/myoepithelial cell layer (K5deltaNbetacat strain) develop mammary hyperplasias that progress to invasive carcinomas. Histological and microarray analyses of these lesions have revealed their high similarity to a subset of basal-like human breast tumours with squamous differentiation. As in human basal-like carcinomas, the Myc pathway was found to be activated in the mammary lesions of K5deltaNbetacat mice. Mammosphere and transplantation assays showed that a basal cell population with stem/progenitor characteristics was amplified in K5deltaNbetacat mouse preneoplastic glands. Myc deletion from the mammary basal layer of K5deltaNbetacat mice abolished both basal cell regenerative capacity and tumorigenesis. These results show that Myc is essential for beta-catenin-induced stem cell amplification and tumorigenesis and that basal stem/progenitor cells may be at the origin of a subset of basal-like breast tumours. mammary tissue from K5M-NM-^TNM-NM-2cat mice were dissected at successive stages of development (small hyperplasia (n=5), large hyperplasia (n=5), tumor (n=11) and control (n=4)) for RNA extraction and hybridization on Affymetrix microarrays

2013-12-31 | E-GEOD-43825 | biostudies-arrayexpress

RNA-sequencing and ChIP-sequencing in murine mesenchymal stem cells treated with Ezh2 inhibitor GSK126 or β-catenin siRNA

Project description:During mesenchymal stem cell (MSC) differentiation, both Wnt signaling and the development of a rigid cytoskeleton promote commitment to the osteoblastic over adipogenic lineage. β-catenin is thought to play a critical role in Wnt effects. We show that β-catenin was additive with cytoskeletal signals to prevent adipogenesis, and β-catenin knockdown promoted adipogenesis even when the actin cytoskeleton was depolymerized. β-catenin also prevented osteoblast commitment in a cytoskeletal-independent manner, with β-catenin knockdown enhancing lineage commitment. Chip-seq showed that β-catenin associated with the promoter of EZH2, a key component of the PRC2 complex that governs genome methylation. Knocking down β-catenin lowered EZH2 levels and H3K27me3 at osteogenic loci. Further, when EZH2 was inhibited, β-catenin ’s anti-differentiation effects were lost. These results indicate that regulating EZH2 activity is key to β-catenin effects on MSC to preserve MSC multipotentiality.

2019-10-17 | GSE138980 | GEO

Gonadal Identity in the Absence of pro-Testis Factor SOX9 and pro-Ovary Factor beta-catenin

Project description:The main goal of our study is to identify the molecular events that determine the gonadal identity in mammals. Although testis and ovary arise from a common embryonic primordium, they represent outcomes of opposing fate determination. This decision to differentiate into a testis or an ovary hinges upon the balance between two antagonizing factors, pro-testis SOX9 and pro-ovary β-catenin. This microarray analysis led to the identification of the genes involved in the fate of XX and XY gonads in absence of SOX9 and beta-catenin We developed mouse genetic models that lack either Sox9, β-catenin, or both specifically in the somatic cells. All embryos used in this study resulted from the crossing between Ctnnb1f/f; Sox9f/f females with Sf1-cre+/Tg ; Ctnnb1+/f; Sox9+/f males. XX and XY fetal gonads were collected at embryonic day E14.5

2015-05-26 | E-GEOD-67463 | biostudies-arrayexpress

KrasG12D partially compensates for the loss of beta-catenin in MLL-AF9 AML

Project description:The Wnt/beta-catenin pathway is required for the development of leukemia stem cells in MLL-AF9 AML. We evaluated the dependance on beta-catenin for KrasG12DMLL-AF9 leukemia. Lin-Kit+ bone marrow cells obtained from mice transplanted with primary MLL-AF9 leukemia cells and KRasG12DMLL-AF9 leukemia cells were assessed for gene expression in the presence or absence of beta-catenin

2014-07-02 | E-GEOD-49248 | biostudies-arrayexpress

Mst1-mediated phosphorylation of FoxO1 and C/EBP-β Stimulates Cell-protective Mechanisms in Cardiomyocytes

Project description:The molecular mechanisms by which FoxO transcription factors mediate diametrically opposite cellular responses, namely death and survival, remain unknown. Mst1 phosphorylates FoxO1 Ser209/Ser215/Ser218/Thr228/Ser232/Ser243, thereby inducing nuclear translocation of FoxO1 in cardiomyocytes. Mst1 inhibits the FoxO1-mediated transcription of proapoptotic genes but promotes that of prosurvival genes. Mst1 increases FoxO1-C/EBP-β interaction and phosphorylates C/EBP-β at Thr299, thereby promoting transcription of prosurvival genes. Myocardial ischemia/reperfusion (I/R) injury was larger in cardiac-specific FoxO1 knockout (c-FoxO1–/–) mice than in control mice. However, the concurrent presence of C/EBP-β T299E phospho-mimetic mutation reduced infarct size in c-FoxO–/– mice. The C/EBP-β phospho-mimetic mutant exhibited a higher binding to the promoter of prosurvival genes compared to wild-type C/EBP-β. In conclusion, phosphorylation of FoxO1 by Mst1 inhibits the binding of FoxO1 to pro-apoptotic gene promoters but enhances its binding to C/EBP-β, phosphorylation of C/EBP-β, and transcription of prosurvival genes, which stimulate protective mechanisms in the heart.

2022-09-12 | GSE213010 | GEO

Transcription profiling of mouse kideney FROM beta catenin deficient animals vs controls AT E12.5

Project description:We generated a murine genetic model of beta-catenin deficiency targeted to the ureteric bud cell lineage to study the role of beta-catenin mediated Wnt signaling during ureteric morphogenesis. Experiment Overall Design: A comparison was made between triplicate samples of E12.5 kidneys from either normal mice or mice with a b-catenin allele containing LoxP sites flanking exons 2 through 6 crossed to Hoxb7-Cre:Gfp mice

2008-04-04 | E-GEOD-9629 | biostudies-arrayexpress

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