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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse hematopoietic cells, Ikaros wt and null mutant

ABSTRACT: Regulation of lineage potential and transcriptional priming by Ikaros. New insight is provided into a bivalent regulation of lineage priming in the HSC and its lympho-myeloid restricted progeny the LMPP by the lymphoid lineage-determining factor Ikaros; Whereas Ikaros is responsible for the activation of a cascade of lymphoid expression programs and for the establishment of lymphoid potential from the HSC to the LMPP it is also responsible for the repression of stem cell and erythroid genetic programs that are incompatible with further lineage restrictions emanating from the LMPP Experiment Overall Design: Ikaros null versus wt

ORGANISM(S): Mus musculus

SUBMITTER: Jiangwen Zhang

PROVIDER: E-GEOD-15330 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression data from mouse hematopoietic cells, Ikaros wt and null mutant

Project description:Regulation of lineage potential and transcriptional priming by Ikaros. New insight is provided into a bivalent regulation of lineage priming in the HSC and its lympho-myeloid restricted progeny the LMPP by the lymphoid lineage-determining factor Ikaros Whereas Ikaros is responsible for the activation of a cascade of lymphoid expression programs and for the establishment of lymphoid potential from the HSC to the LMPP it is also responsible for the repression of stem cell and erythroid genetic programs that are incompatible with further lineage restrictions emanating from the LMPP Keywords: Ikaros null versus wt

2009-04-03 | GSE15330 | GEO

High levels of canonical Wnt signaling lead to loss of stemness and increased differentiation in hematopoietic stem cells

Project description:Canonical Wnt signalling regulates the self-renewal of most if not all stem cell systems. In the blood system, the role of Wnt signalling has been subject of much debate, with positive and negative roles of Wnt signalling proposed for hematopoietic stem cells (HSC). As we have shown previously, this controversy can be largely explained by the effects of different dosages of Wnt signalling. What remained unclear however, was why high Wnt signals would lead to loss of reconstituting capacity. To better understand this phenomenon, we have taken advantage of a series of hypomorphic mutant Apc alleles resulting in a broad range of Wnt dosages in HSCs, purified those HSCs and performed whole genome gene expression analyses. Gene expression profiling and functional studies show that HSCs with APC mutations lead to high Wnt levels , enhanced differentiation and diminished proliferation, but have no effect on apoptosis, collectively leading to loss of stemness. Thus, we provide mechanistic insight into the role of APC mutations and Wnt signalling in HSC biology. As Wnt signals are explored in various in vivo and ex vivo expansion protocols for HSCs, our findings also have clinical ramifications. To investigate the effects of Wnt signals in hematopoietic cells, mice carrying floxed Apc or hypomorphic Apc mutants were crossed, LSK cells were isolated and treated with Cre IRES GFP gamma-retrovirus ex vivo, GFP+ cells were sorted and RNA expression was determined.

2016-03-23 | E-GEOD-79495 | biostudies-arrayexpress

Gene expression in WT and Ikaros-deficient LSK cells

Project description:The Ikaros zink finger transcription factor is a critical regulator of the hematopietic system, and plays an important role in the regulation of the development and function of several blood cell lineages. We used microarrays to characterize how Ikaros deficieny affects global transcription in the hematopoietic stem and progenitor cells from wild-type and Ikaros mutant mice. lin- Sca1+ c-Kit+ (LSK) cells, that contains the hematopoietic stem cells and the multipotent progenitor cells, were sorted by FACS from the bone marrow of 6-7 weeks old WT and IkL/L mutant mice. Total RNA extracted from these cells was subjected to transcriptome analysis.

2015-11-03 | E-GEOD-61147 | biostudies-arrayexpress

Gene expression profiles of Lkb1 WT and KO hematopoietic stem cells (HSCs)

Project description:LKB1 encodes a Ser/Thr kinase and acts as an evolutionarily conserved sensor of cellular energy status in eukaryotic cells. LKB1 functions as the major upstream kinase to phosphorylate AMPK and 12 other AMPK-related kinases, which is required for their activation in many cellular contexts. Once activated, AMPK and AMPK-related kinases phosphorylate a diverse array of downstream effectors to switch on ATP-generating catabolic processes and switch off ATP-consuming anabolic processes, thus restoring energy balance during periods of energetic stress. To study the role and mechanisms of Lkb1 in the regulation of hematopoietic stem cell (HSC) biology, we performed transcriptome analysis of sorted LSK (Lin-, Sca-1+, c-Kit+) cells from Lkb1 WT and KO bone marrows at 1 day post-completing tamoxifen injection (DPI). To identify more proximal molecular effects, we chose 1 DPI due to the modest phenotypes in Lkb1 KO mice, yet documentation of efficient Lkb1 deletion in LSK cells at this very early time point. We treated Lkb1 L/L rosa26CreERT2 and Lkb1 L/L mice (C57BL/Ka-CD45.2:Thy-1.1 background) with Tamoxifen for 5 days to somatically delete Lkb1 in adult mice, and generated Lkb1 WT and KO mice. At 1 DPI, we prepared single-cell suspensions from bone marrow (from femoral and tibial bones), and stained and sorted LSK populations using FACSAria (Becton Dickinson, Mountain View, CA). The RNA was extracted from sorted LSK cells, amplified and subjected to gene profiling. The samples include 3 Lkb1 WT (Lkb1 WT 5-7) and 4 Lkb1 KO (Lkb1 KO 4-7) replicates.

2010-12-01 | E-GEOD-24765 | biostudies-arrayexpress

Gene expression in mouse pre-B cells transduced with Ikaros.

Project description:Ikaros family DNA binding proteins are critical regulators of B cell development. To identify Ikaros-regulated genes in pre-B cells we performed gene expression studies at enhanced temporal resolution. We used retroviral gene transfer to express Ikaros proteins in the pre-B cell line B3. Total RNA from 2 biological replicates of B3 cells transduced with wild type Ikaros (HA-Ikaros-IRES-GFP) and DNA binding-deficient Ikaros mutant 159A (HA-159A Ikaros-IRES-GFP) was isolated 48h after infection. To increase the temporal resolution of Ikaros-regulated gene expression we transduced B3 cells with inducible Ikaros (HA-Ikaros-ERt2-IRES-GFP) and isolated total RNA from 3 biological replicates after 2 h and 6 h of exposure to 4-hydroxytamoxifen. Vector transduced B3 cells (ERt2-IRES-GFP) treated with 4-hydroxytamoxifen were used as controls.

2013-01-15 | E-GEOD-38110 | biostudies-arrayexpress

Genome-wide identification of Ikaros binding sites in pre-B cells

Project description:Ikaros DNA binding proteins are important regulators of haematopoiesis and genetic deletion of Ikaros results in severe developmental disturbances, including delayed thymocyte differentiation and an early and complete block in B cell development. Although Ikaros ChIP-seq data are available for mouse thymocytes and human haematopoietic progenitors, it has not been achieved in B cell progenitors. The goal of this study was to identify Ikaros binding sites in pre-B cells to define Ikaros target genes which could explain the essential role of Ikaros proteins in B cell differentiation. We carried out chromatin immunoprecipitation and high throughput sequencing (ChIP-seq) with antibodies to the C-terminus of endogenous Ikaros in B3 cells and with anti-haemagglutinin (HA) in B3 cells transduced with epitope-tagged HA-Ikaros.

2013-01-15 | E-GEOD-38169 | biostudies-arrayexpress

Gene expression in mouse primary pre-B cells transduced with Ikaros

Project description:Ikaros family DNA binding proteins are critical regulators of B cell development. To identify Ikaros-regulated genes in primary pre-B cells we performed gene expression microarrays. We used retroviral gene transfer to express Ikaros proteins. Total RNA from 3 biological replicates of primary pre-B cells transduced with wild type Ikaros (HA-Ikaros-IRES-GFP) and control vector (IRES-GFP) was isolated 48h after infection.

2013-01-15 | E-GEOD-42551 | biostudies-arrayexpress

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells following Ikaros restoration

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells isolated from two untreated and two 3-day Dox-treated mice.

2015-02-02 | E-GEOD-64899 | biostudies-arrayexpress

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL65) cells following Ikaros restoration

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL65) cells isolated from three untreated and three 3-day Dox-treated mice. There were two sequencing runs of each RNA sample.

2015-02-02 | E-GEOD-64893 | biostudies-arrayexpress

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL101) cells following Ikaros restoration [RNA-Seq]

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL101) cells isolated from three untreated and three 3-day Dox-treated mice. There were two sequencing runs of each RNA sample.

2015-02-02 | E-GEOD-54447 | biostudies-arrayexpress

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