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Effect of Ikaros deletion on gene expression in CD4 T cells

ABSTRACT: The goal of this experiment is to define how lack of Ikaros impacts gene expression in mature CD4 T cells, both in the resting and activated state. To do this, a conditional knockout mouse model was generated using Cre/lox technology. The floxed allele was designed such that the last translated exon and 3' UTR of the Ikaros gene (Ikzf1) are deleted in mature T cells (mediated by distal Lck-driven Cre). CD4 T cells from mice with floxed alleles that did not express Cre (Cre-) and those that did express Cre (Cre+) were analyzed.

ORGANISM(S): Mus musculus

PROVIDER: GSE119067 | GEO | 2018/12/12

REPOSITORIES: GEO

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Splenic B1 and B2 cells from mice with induced deletion of Ikaros

Project description:The experiment aimed at determining the genes that are under the control of the Ikaros transcription factor in mouse splenic B1 and B2 B lymphocyte subsets. To this aim, we used Ikf/f R26-CreERT2+ (Cre+) or Ikf/f R26-CreERT2- (Cre-) mice, which correspond to mice with floxed null alleles for Ikzf1 (Heizmann et al., JEM 210:2823-32, 2013) that were crossed with the R26-CreERT2 mice, which harbor a knock-in of the cDNA encoding the tamoxifen (TAM) inducible CreERT2 recombinase in the Rosa26 gene (Badea et al, J. Neurosci 23:2314-22, 2003). 6-8 week-old mice were injected daily with TAM for 3d (50mg/kg). Mice were sacrificed 10d after the first injection, and splenic B1 and B2 B cell populations sorted by flow cytometry. Splenic B1 and B2 cells from mice with induced deletion of Ikaros

2016-02-03 | GSE75827 | GEO

RNA-SEQ analysis of CD4+ T cells in presence or absence of Ikaros.

Project description:We found by microarray analysis that Ikaros is critical to limit the expression of several pro-inflammatory genes during Th17 cell polarization. To unravel the role of Ikaros in the expression of pro-inflammatory genes without Th17 polarizing cytokines, we performed an RNA-seq analysis in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies (Th0 condition), from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+).

2021-04-26 | GSE157810 | GEO

Ikaros deficient mouse thymic lymphomas

Project description:This dataset comprises expression profiles from 3 thymic lymphomas from Ikaros deficient mice (IkL/L model, see Dumortier et al, Mol. Cell. Biol. 26, 209-220, 2006 for a description of the tumor model) and 3 thymic lymphomas from IkL/L mice that harbor a mutation of the Notch1 gene (deletion of floxed sequences comprising the promoter and exon 1 with the CD4-Cre transgene). The results from this experimpent is that the expression of Notch target genes was unexpectedly not altered in the tumors with the Notch1 deletion. This result is explained by the activation of a cryptic 3' Notch1 promoter in the deleted tumors, which leads to constitutive Notch1 activation. These results are described in the following publication: R Jeannet, J Mastio, B Macias-Garcia, A Oravecz, T Ashworth, AS Geimer-Lelay, B Jost, S Le Gras, J Ghysdael, T Gridley, T Honjo, F Radtke, J Aster, S Chan and P Kastner. Oncogenic activation of the Notch1 gene in mouse T-cell leukemia by deletion of its promoter. Blood, in press (2010) Primary thymic tumors from 3 IkL/L Notch1+/+ CD4-Cre+ mice (aged 18-20 weeks) were compared to similar tumors from 3 IkL/L Notch1f/f CD4-Cre+ mice (aged 8-10 weeks).

2010-09-03 | E-GEOD-23972 | biostudies-arrayexpress

Genome wide chromatin accessibility (ATAC-SEQ) in the presence or absence of Ikaros in CD4+ T cells.

Project description:We found that Ikaros is critical to limit the expression of pro-inflammatory cytokines in TCR/CD28-activated CD4+ T cells. To understand if Ikaros could modify the chromatin accessibility in regions controling the expression of these pro-inflammatory genes, we examined the chromatin state in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies for 1 and 2 days, from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+), using the ATAC-seq approach.

2021-04-26 | GSE157812 | GEO

Stage-specific control of early B cell development by the transcription factor Ikaros

Project description:Ikaros is an essential regulator of lymphopoiesis. Here, we studied the B-cell-specific function of Ikaros by conditional Ikzf1 inactivation in pro-B cells. B-cell development was arrested at an aberrant ‘pro-B’ cell stage characterized by increased cell adhesion and loss of pre-B cell receptor signaling. Ikaros was found to activate genes coding for pre-BCR signal transducers and to repress genes involved in the downregulation of pre-BCR signaling and upregulation of the integrin signaling pathway. Unexpectedly, derepression of Aiolos expression could not compensate for the loss of Ikaros in pro-B cells. Ikaros differentially controlled active chromatin at promoters and enhancers of repressed and activated target genes. Notably, Ikaros binding and target gene expression was dynamically regulated at distinct stages of early B-lymphopoiesis. 16 RNA-Seq samples in pre-proB cells (4 replicates, for each 2 controls and 2 experimental samples); 4 RNA-Seq samples in pro-B cells in Rag2-/- backgrounds (Ikzf1 deleted versus non deleted, 2 replicates each); 4 RNA-Seq samples in c-Kit high pro-B cells (Ikzf1 deleted versus non deleted, 2 replicates each); 4 RNA-Seq samples in pro-B cells (Ikzf1 deleted versus non deleted, 2 replicates each); 2 RNA-Seq samples pre-B cells wild type; 8 chromatin ChIP-Seq samples (4x H3K9ac, 4x H3K4me3, Ikzf1 deleted/non deleted, two replicates each).; 4 Transcription factor ChIP-Seq samples in pro-B cells; 1 Transcription factor ChIP-Seq samples in DP-T cells; 1 Transcription factor ChIP-Seq samples in pre-pro-B cells; 2 Mi-2b Chip-Seq samples (Ikzf1 deleted versus non deleted); 1 ChIP-Seq input track for pro-B cells; 1 ChIP-Seq input track for DP-T cells

2014-02-09 | E-GEOD-53595 | biostudies-arrayexpress

Ikaros is a principal regulator of Aire+ mTEC homeostasis, thymic mimetic cell diversity, and central tolerance [Ikaros scATAC-seq]

Project description:The zinc-finger transcription factor Ikaros (Ikzf1) modulates key gene expression programs important for hematopoietic development, and coding mutations in IKZF1 are found in patients with immunodeficiency, leukemia, and autoimmunity. While Ikaros has a well-established function in hematopoiesis, its role in other cell types is less well defined. Here, we uncover new functions for Ikaros in thymic epithelial lineage development and show that Ikzf1 expression in medullary thymic epithelial cells (mTECs) is required for both Autoimmune Regulator positive (Aire+) mTEC development and tissue-specific antigen (TSA) gene expression. Accordingly, TEC-specific deletion of Ikzf1 in mice results in a profound decrease in Aire+ mTECs, a global loss of TSA gene expression, and the development of autoimmunity. Moreover, Ikaros shapes thymic mimetic cell diversity and its deletion results in a dramatic expansion of thymic tuft cells and muscle-like mTECs and a loss of other Aire-dependent mimetic populations. Single-cell analysis reveals Ikaros modulates core transcriptional programs in TECs that correlate with the observed cellular changes. Our findings highlight a previously undescribed role for Ikaros in regulating epithelial lineage development and function, and suggest that failed thymic central tolerance could contribute to the autoimmunity seen in humans with IKZF1 mutations.

2023-10-25 | GSE238149 | GEO

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ATAC-Seq]

Project description:Using patient-derived Ph+ pre-B ALL cells that harbor deletions of the IKZF1 DNA binding domain (Ik6), we performed ATAC-sequencing in cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

2017-02-06 | GSE90666 | GEO

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ChIP-seq]

Project description:ChIP-seq was performed in patient-derived BCR-ABL1+ (Ph+) pre-B ALL cells that harbor heterozygote deletions of the IKZF1 DNA binding domain (Ik6), using cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

2017-02-06 | GSE90656 | GEO

Ikaros mutation confers integrin-dependent pre-B cell survival and progression to acute lymphoblastic leukemia

Project description:Deletion of the Ikaros DNA-binding domain generates dominant-negative isoforms that interfere with Ikaros family activity and correlate with poor prognosis in human precursor B cell acute lymphoblastic leukemias (B-ALL). Here, we show that conditional inactivation of the Ikaros DNA binding domain in early pre-B cells arrests their differentiation at a stage where integrin-dependent niche adhesion augments mitogen-activated protein kinase signaling, proliferation, and self-renewal, and attenuates pre-B cell receptor signaling and differentiation. Transplantation of polyclonal Ikzf1 mutant pre-B cells results in long-latency oligoclonal pre-B-ALL, demonstrating that loss of Ikaros contributes to multistep B-leukemogenesis. These results explain how normal pre-B cells transit from a highly proliferative and stromal-dependent to a stromal-independent phase where differentiation is enabled, providing potential therapeutic strategies for IKZF1 mutant B-ALL. One of the analyses described in this manuscript is the differential gene expression of large preB cells sorted from the bone marrow of WT and IKDN mice. The RNASeq method and Deseq analysis algorithm were employed

2014-02-09 | E-GEOD-53401 | biostudies-arrayexpress

Ikaros is a principal regulator of Aire+ mTEC homeostasis, thymic mimetic cell diversity, and central tolerance (scRNA seq)

2023-10-25 | GSE241742 | GEO

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