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Effect of Evi-1 deletion in hematopoietic stem cells

ABSTRACT: To identify the target genes of Evi-1 in hematopoietic stem cells (HSCs), we carried out genome-wide transcriptional analysis using wild-type and Evi-1-deleted HSCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE11557 | GEO | 2008/05/29

SECONDARY ACCESSION(S): PRJNA106289

REPOSITORIES: GEO

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Transcription profiling of mouse Evi-1 deleted hematopoietic stem cells

Project description:To identify the target genes of Evi-1 in hematopoietic stem cells (HSCs), we carried out genome-wide transcriptional analysis using wild-type and Evi-1-deleted HSCs. Experiment Overall Design: Lineage(-), Sca-1(+), c-Kit(+) cells derived from Evi-1(flox/flox) mice were transduced with GFP or Cre-GFP expressing retroviruses. GFP(+) cells were sorted and and analyzed by AffymetrixÂ® Mouse Genome 430 2.0 ArrayÂ® for gene expression. Two independent experiments were performed.

2008-06-19 | E-GEOD-11557 | biostudies-arrayexpress

Identification of endothelial genes co-regulated upon endothelial Evi/Wls and Rspo3 deletion

Project description:Inducible endothelial Rspo3 deletion resulted in perturbed developmental and tumor vascular remodeling. Rspo3-iECKO mice strikingly phenocopied the non-canonical WNT signaling-induced vascular defects of mice deleted for the WNT secretion factor Evi/Wls. An endothelial screen for RSPO3 and EVI/WLS co-regulated genes identified novel target genes, which could be linked to WNT/Ca2+/NFAT signaling. In summary, the study identifies endothelial RSPO3-driven non canonical WNT/Ca2+/NFAT signaling as critical maintenance pathway of the remodeling vasculature.

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Igf2bp2 deletion reduces energy metabolism, gIgf2bp2 deletion reduces energy metabolism, growth signaling, and aging of hematopoietic stem cells in micerowth signaling, and aging of hematopoietic stem cells in mice

Project description:Increasing evidence links metabolic activity and cell growth to decline in hematopoietic stem cell (HSC) function during aging. The Lin28b/Hmga2 pathway controls tissue development and in the hematopoietic system the postnatal downregulation of this pathway causes a decrease in self renewal of adult HSCs compared to fetal HSCs. Igf2bp2 is an RNA binding protein and a mediator of the Lin28b/Hmga2 pathway, which regulates metabolism and growth signaling by influencing RNA stability and translation of its target genes. It is currently unknown whether Lin28/Hmga2/Igf2bp2 signaling impacts on aging-associated impairments in HSC function and hematopoiesis. Here, we analyzed homozygous Igf2bp2 germline knockout mice and wildtype control animals to address this question. The study shows that Igf2bp2 deletion rescues aging phenotypes of the hematopoietic system, such as the expansion of HSC numbers in bone marrow and the biased increase of myeloid cells in peripheral blood. This rescue of hematopoietic aging coincides with reduced mitochondrial metabolism and glycolysis in Igf2bp2-/- HSCs compared to Igf2bp2+/+ HSCs. Conversely, Igf2bp2 overexpression activates protein synthesis pathways in HSCs and leads to a rapid loss of self renewal by enhancing myeloid skewed differentiation in an mTOR/PI3K-dependent manner. Together, these results show that Igf2bp2 regulates energy metabolism and growth signaling in HSCs and that the activity of this pathways influences self renewal, differentiation, and aging of HSCs.

2024-05-21 | PXD018535 | Pride

Analysis of Evi-deficient teratoma

Project description:expression analysis of teratoma, grown from mouse embryonic stem cells that are Evi/Wls knockout cells and comparison with wildtype (control) tumors

2014-12-10 | E-MTAB-2927 | biostudies-arrayexpress

Wnt secretion protein Evi/Gpr177 promotes glioma tumorigenesis

Project description:Silencing of Evi and beta-catenin in U87MG cells

2012-06-29 | E-MTAB-776 | biostudies-arrayexpress

RNAseq transcriptomic signature associated depletion of Evi/Wls in epidermal sheets of mice, expression analysis of epidermal sheets of Evi/Wls knockout and wildtype mice

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2013-07-24 | E-MTAB-1613 | biostudies-arrayexpress

Late fetal hematopoietic failure results from ZBTB11 deficiency despite abundant HSC specification

Project description:We have used a conditional mouse model to investigate the role of Zbtb11 specifically in hematopoiesis. When Zbtb11 was deleted in the hematopoietic compartment, embryos died at embryonic day E18.5 with hematopoietic failure. Zbtb11 hematopoietic knockout (Zbtb11hKO) hematopoietic stem cells (HSCs) were overabundantly specified at E14.5 through E17.5 compared to controls. Overspecification was accompanied by loss of stemness, inability to differentiate into committed progenitors and mature lineages in fetal liver, failure to seed fetal bone marrow and total hematopoietic failure. Zbtb11hKO HSCs did not proliferate in vitro and were constrained in cell cycle progression, demonstrating a cell-intrinsic role for Zbtb11 in proliferation and cell cycle regulation in mammalian HSCs. scRNAseq analysis identified Zbtb11-deficient HSCs were underrepresented in an erythroid-primed subpopulation and showed downregulation of oxidative phosphorylation (OXPHOS) pathways and dysregulation of genes associated with the hematopoietic niche. We have identified a cell-intrinsic requirement for Zbtb11-mediated gene regulatory networks in sustaining a pool of maturation-capable hematopoietic stem and progenitor cells.

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Arrayexpression analysis of Evi-overexpressing teratomas

Project description:Canonical and non-canonical Wnt signaling play key roles during development and tumorigenesis. In this study we compared gene expression in teratomas grown from mouse embryonic stem cells that overexpress Evi/Wls and teratomas from normal embryonic stem cells cells.

2016-03-06 | E-MTAB-3995 | biostudies-arrayexpress

Rad21-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation

Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

2018-11-28 | PXD011537 | Pride

Mitochondrial respiratory chain is essential for hematopoietic stem cell function

Project description:Adult and fetal hematopoietic stem cells (HSCs) display a glycolytic phenotype, which is required for maintenance of stemness; however, whether mitochondrial respiration is required to maintain HSC function is not known. Here we report that loss of the mitochondrial complex III subunit Rieske iron sulfur protein (RISP) in fetal mouse HSCs allows them to proliferate but impairs their differentiation, resulting in anemia and prenatal death. RISP null fetal HSCs displayed impaired respiration resulting in a decreased NAD+/NADH ratio. RISP null fetal HSCs and progenitors exhibited an increase in both DNA and histone methylation concomitant with increases in 2-hydroxyglutarate (2-HG), a metabolite known to inhibit DNA and histone demethylases. RISP inactivation in adult HSCs also impaired respiration resulting in loss of quiescence resulting in severe pancytopenia and lethality. Thus, respiration is dispensable for adult or fetal HSC proliferation, but essential for fetal HSC differentiation and maintenance of adult HSC quiescence.

2017-09-13 | PXD006054 | Pride

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