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Expression data from RUNX1S291fs-mutant and/or Ezh2 conditional knockout Lineage-c-Kit+Sca-1+ (LSK) cells

ABSTRACT: Recent studies have showed that loss-of-function mutations of EZH2, a catalytic component of polycomb repressive complex 2, are often associated with RUNX1 mutations in myelodysplastic syndrome (MDS) patients. We established a novel MDS model mouse by transducing a RUNX1S291fs mutant in hematopoietic stem cells followed by deletion of Ezh2 and found that Ezh2 loss significantly promoted RUNX1S291fs-induced MDS.

ORGANISM(S): Mus musculus

PROVIDER: GSE50537 | GEO | 2013/09/04

SECONDARY ACCESSION(S): PRJNA217910

REPOSITORIES: GEO

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Expression data from RUNX1S291fs-mutant and/or Ezh2 conditional knockout Lineage-c-Kit+Sca-1+ (LSK) cells

Project description:Recent studies have showed that loss-of-function mutations of EZH2, a catalytic component of polycomb repressive complex 2, are often associated with RUNX1 mutations in myelodysplastic syndrome (MDS) patients. We established a novel MDS model mouse by transducing a RUNX1S291fs mutant in hematopoietic stem cells followed by deletion of Ezh2 and found that Ezh2 loss significantly promoted RUNX1S291fs-induced MDS. We retrovirally transduced RUNX1S291fs or empty-control into either Cre-ERT;Ezh2wt/wt or Cre-ERT;Ezh2flox/flox (CD45.2+) HSCs. The transduced cells were transplanted into lethally irradiated recipient mice together with life-saving CD45.1+ wild-type bone marrow cells. After deletion of Ezh2, gene expression analysis were performed on pooled bone marrow LSK cells isolated from WT, Ezh2Δ/Δ, RUNX1S291fs, and RUNX1S291fs/Ezh2Δ/Δ mice (n=2-4) and two distinct RUNX1S291fs/Ezh2Δ/Δ-MDS mouse.

2013-09-04 | E-GEOD-50537 | biostudies-arrayexpress

Expression data from diseased Ezh2 KO Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

Project description:Recent studies have shown that epigenetic regulator are mutated in myelodysplastic syndrome (MDS) patients. Ezh2 is frequently mutated in hematopoietic malignant patients, however, the pathophysiological role of Ezh2 mutations has not been elucidated yet. In this study, we examined the function of Ezh2 in murine hematopoietic disease. Ezh2 deleted mice with myeloid malignancies including MDS, Myelodysplasia/myeloneoplasm(MDS/MPN), Myelodysplasia/myeloneoplasm_thrombocytosis(MDS/MPN_TC)

2015-03-14 | GSE66897 | GEO

Expression data from Sf3b1 heterozygous Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

2013-09-20 | GSE51038 | GEO

Expression data from Sf3b1 heterozygous Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

Project description:Recent studies have shown that multiple components of the mRNA splicing machinery are mutated in myelodysplastic syndrome (MDS) patients. SF3B1 is frequently mutated in refractory anemia with ringed sideroblasts (RARS)-MDS patients, however, the pathophysiological role of SF3B1 mutations has not been elucidated yet. In this study, we examined the function of Sf3b1 in murine hematopoiesis. Since Sf3b1 null homozygotes died during preimplantation development, in this study, we utilized Sf3b1 heterozygous mice showing grossly normal growth. We harvested bone marrow stem/progenitor (LSK) cells from wild type (WT) and Sf3b1+/- mice (n=4) at 20 weeks old. In addition, to exclude the possibility of indirect effect from bone marrow environment, we transplanted total bone marrow cells from WT or Sf3b1+/- (CD45.2+) mice into lethally irradiated CD45.1+ recipient mice, and then harvested (CD45.2+) LSK cells from the recipients (n=5) at 9 months-post transplantation.

2013-09-20 | E-GEOD-51038 | biostudies-arrayexpress

H3K27me3 ChIP-sequencing on LSK (Lin-Sca-1+c-kit+) cells isolated from control, MxCre Jak2VF/+ and MxCre Jak2VF/+ EZH2-/- mice

Project description:Inactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To identify the Ezh2 target genes that are regulated by H3K27me3 in MF, we performed H3K27me3 ChIP-sequencing in sorted LSK cells from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.

2016-04-19 | GSE79319 | GEO

Expression data from Lineage-c-Kit+Sca-1+ (LSK) and megakaryocyte/erythroid progenitor (MEP) cells isolated from JAK2V617F/Ezh2Δ/Δ mice post JQ1 treatment

2015-06-04 | GSE69499 | GEO

Expression data from Lineage-c-Kit+Sca-1+ (LSK) and megakaryocyte/erythroid progenitor (MEP) cells isolated from JAK2V617F/Ezh2?/? mice post JQ1 treatment

Project description:Loss-of-function mutations in EZH2 are associated with worse outcomes in patients with primary myelofibrosis (PMF). To understand how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for Ezh2 conditional deletion and a JAK2V617F transgene. The total bone marrow cells isolated from JAK2V617F;Ezh2flox/flox;Cre-ERT2 mice were transplanted into lethally irradiated CD45.1+ wild-type recipient mice. Post the deletion of Ezh2, we administered JAK2V617F/Ezh2?/? mice with JQ1 or control DMSO for two weeks, and performed gene-expression analysis of bone marrow LSKs and MEPs immediately after completion of JQ1 treatment.

2015-06-04 | E-GEOD-69499 | biostudies-arrayexpress

Expression data from Lineage-c-Kit+Sca-1+ (LSK) and megakaryocyte/erythroid progenitor (MEP) cells isolated from WT, Ezh2Δ/Δ, JAK2V617F, and JAK2V617F/Ezh2Δ/Δ mice

2015-06-04 | GSE69498 | GEO

Expression data from Bone marrow and Fetal liver Lineage-c-Kit+Sca-1+ (LSK) cells

Project description:Loss of polycomb-group gene Ezh2 causes activation of fetal gene signature in adult mouse bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs). Ezh2 directly represses fetal-specific let-7 target genes, including Lin28, thereby cooperates with let-7 microRNAs in silencing fetal gene signature in BM HSPCs.

2015-08-27 | GSE69760 | GEO

Expression data from Lineage-c-Kit+Sca-1+ (LSK) and megakaryocyte/erythroid progenitor (MEP) cells isolated from WT, Ezh2?/?, JAK2V617F, and JAK2V617F/Ezh2?/? mice

Project description:Loss-of-function mutations in EZH2 are associated with worse outcomes in patients with primary myelofibrosis (PMF). To understand how EZH2 insufficiency is involved in the pathogenesis of PMF, we generated mice compound for Ezh2 conditional deletion and a JAK2V617F transgene. The total bone marrow cells isolated from Cre-ERT2, Ezh2flox/flox;Cre-ERT2, JAK2V617F;Cre-ERT2 and JAK2V617F;Ezh2flox/flox;Cre-ERT2 mice were transplanted into lethally irradiated CD45.1+ wild-type recipient mice. As we deleted Ezh2 at four weeks post transplantation, we performed gene-expression analysis of LSKs and MEPs isolated from the recipient mice at 2 months post transplantation.

2015-06-04 | E-GEOD-69498 | biostudies-arrayexpress

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