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Gene expression profiling to study the transcriptional consequences of Jak2V617F expression and/or Tet2 loss in murine hematopoietic stem cells

ABSTRACT: To interrogate the molecular pathways disrupted by Jak2V617F expression and/or Tet2 loss, Lin-negative, Sca-1-positive, c-kit-positive (LSK) hematopoietic progenitor cells were isolated from bone marrow of wild-type, Jak2V617F, Tet2-null or Jak2V617F/Tet2-null animals (n= 2-4 mice per group) and subjected to gene expression profiling.

ORGANISM(S): Mus musculus

SUBMITTER: Edwin Chen

PROVIDER: E-MTAB-2986 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from loss-of-TET2 and/or JAK2V617F mutant Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

Project description:Recent studies have shown that both TET2 mutation and JAK2V617F mutation are frequent in myeloproliferative neoplasms patients. The pathophysiological roles of each mutation have been elucidated in murine models, but the cooperative effect of the two mutations has not been elucidated yet. In this study, we examined the function of the cooperative effect of loss-of-TET2 function and JAK2V617F mutation in murine hematopoiesis. In this study, we utilized wild type (WT) mice, TET2 knock down (TET2KD) mice, JAK2V617F transgenic mice, double mutant mice. We transplanted 4 types of E14.5 fetal liver cells (WT, TET2KD, JAK2V617F, double mutant) into lethally irradiated mice. At 10-16 weeks post-transplantation, LSK cells from the BM of the recipients were collected, and gene expression analysis was performed. (WT,5 mice at 16 weeks; TET2KD, 5 mice at 10 weeks; JAK2V617F, 5 mice at 16 weeks; double mutant, 5 mice at 13 weeks)

2014-10-16 | E-GEOD-62302 | biostudies-arrayexpress

RNA-seq of Jak2VF LSK cells transduced with Dnmt3a-Cas9-GFP lentivirus vs. emp-Cas9-GFP controls one week and five weeks post methylcellulose plating

Project description:Determination of differentially expressed genes in culture-derived hematopoietic stem cell progenitors (LSK) between Jak2VF-emp-Cas9 and Jak2VF-Dnmt3a-cas9.

2018-10-29 | E-MTAB-6635 | biostudies-arrayexpress

RNA-seq of Jak2VF LSK cells transduced with Dnmt3a-Cas9-GFP lentivirus vs. emp-Cas9-GFP controls 8 weeks post transplantation

Project description:Determination of differentially expressed genes from in vivo hematopoietic stem cell progenitors (LSK) in Jak2VF-emp-Cas9 and Jak2VF-Dnmt3a-Cas9 8 weeks post transplantation.

2018-10-29 | E-MTAB-6644 | biostudies-arrayexpress

ATAC-seq of Jak2VF LSK cells transduced with Dnmt3a-Cas9-GFP lentivirus vs. emp-Cas9-GFP controls 8 weeks post transplantation

Project description:Determination of chromatin accessibility in hematopoietic stem cell progenitors (LSK) of Jak2VF-emp-Cas9 and Jak2VF-Dnmt3a-Cas9 8 weeks post transplantation.

2018-10-29 | E-MTAB-6649 | biostudies-arrayexpress

Expression data from loss-of-TET2 and/or JAK2V617F mutant Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

2014-10-16 | GSE62302 | GEO

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Project description:Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation. These studies show that a ubiquitin ligase-substrate pair can orchestrate the molecular program of HSC differentitiation Gene expression profiles from WT and Tet2-/- sorted LSK and myeloid progenitors (CMP and GMP) were compared using genome wide mRNA expression profiling by Affymetrix genechip arrays (Mouse 430 2.0) and key targets were validated by chromatin immunoprecipitation experiments.

2011-07-01 | E-GEOD-27816 | biostudies-arrayexpress

Tet2-/-Flt3ITD and WT stem and progenitor cells

Project description:The study was a comparison of gene expression using RNA-seq. We analyzed the stem and progenitor cells from WT and Vav-cre+ Tet2fl/fl Flt3-ITD (T2F3) mice. We isolated stem cells LSK (lin- sca+ kit+) and granulocyte-macrophage progenitors GMP (lin- sca- kit+ fcgr+ cd34+) cells from bone marrow. Comparisons were made across genotypes WT vs. T2F3 and cell types LSK vs. GMP. Comparison of WT and Tet2-/-Flt3ITD bone marrow stem and progenitor cells.

2015-05-01 | E-GEOD-57244 | biostudies-arrayexpress

Acute loss of TET function results in aggressive myeloid cancer in mice [WGBS]

Project description:To evaluate the DNA methylation in LSK cells from the bone marrow of wildtype or Tet2/3 DKO mice. In order to address the impact of the loss of Tet2/3 proteins in DNA methylation in LSK cells, we compared by WGBS the methylome of wild and, Tet2/3 DKO LSK cells in bone marrow.

2015-11-26 | E-GEOD-72629 | biostudies-arrayexpress

Gene expression profiling distinguishes JAK2V617F-negative from JAK2V617F-positive patients in essential thrombocythemia

Project description:In order to explore the gene expression signature in essential thrombocythemia (ET) patients in relation to JAK2V617F mutational status, expression profiling in circulating granulocytes was performed. Twenty ET were studied by microarray analysis and the results were confirmed by real-time quantitative RT-PCR in 40 ET patients, not receiving cytoreductive treatment. A heterogeneous molecular signature characterized by two main gene expression patterns was found: one with an up-regulation of inflammatory genes related to neutrophil activation and thrombosis, and the other one with significantly lower expression of these genes. Supervised clustering analysis showed 30 genes differentially expressed between JAK2V617F-negative and JAK2V617F-positive ET patients. Among the JAK2V617F-negative, a set of 14 genes (CISH, C13orf18, CCL3, PIM1, MAFF, SOCS3, ID2, GADD45B, KLF5, TNF, LAMB3, HRH4, TAGAP and TRIB1) showed an abnormal expression pattern. In this group of patients CISH, SOCS2, SOCS3 and PIM1 genes, all involved in JAK-STAT signaling pathway, presented a lower expression,. A two-gene predictor model was built comprising FOSB and CISH genes, which were the best discriminators of JAK2V617F status. In conclusion, JAK2V617F-negative ET patients present a characteristic gene expression profile, different from JAK2V617F-positive patients. Other pathways besides JAK-STAT might be implicated in the pathophysiology of JAK2V617F-negative ET patients. Keywords: Disease state analysis

2008-05-19 | GSE11003 | GEO

Expression changes with JAK2V617F and TNF receptor block in a murine model of MPN

Project description:We analyzed expression changes between JAK2V617F positive bone marrow cells and JAK2V617F negative cells We further analyzed how TNF receptor (receptor 1 or receptor 2) block influenced these changes in JAKV617F positive relative to JAK2V617F negative

2018-07-31 | GSE104792 | GEO

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