GFI1 and IKAROS
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA672152 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12903453.fastq.gz | Fastqsanger.gz | |||
| SRR12903454.fastq.gz | Fastqsanger.gz | |||
| SRR12903455.fastq.gz | Fastqsanger.gz | |||
| SRR12903456.fastq.gz | Fastqsanger.gz | |||
| SRR12903457.fastq.gz | Fastqsanger.gz |
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Project description:To study the interplay between GFI1 and IKAROS in T-cell Acute Lymphoblastic Leukemia (T-ALL), we applied ChIP-Seq to CCRF-CEM cells expressing 3XFLAG-tagged GFI1 OR IKAROS under doxycycline-inducible control.We found these two protiens associated with common genes, including genes associated with T cell development.
2021-10-31 | GSE160181 | GEO
Project description:To identify changes in gene expression associated with either ectopic GFI1 expression or CRISPR-mediated IKAROS knockout, we applied bulk RNA-Seq with GFI1-3XFLAG CCRF-CEM cells. Wild type or IKAROS knockout cells were treated with vehicle or doxycycline for 24 hours. Between 21.7 and 28.2 million RNA-Seq reads were generated for each condition, 88.6 to 90.3% of which aligned uniquely to the human Hg38 reference genome. ~99% of the reads within coding regions aligned to the correct strand. Hierarchically clustering the top 500 most significantly differentially regulated genes across all the conditions (ranked based on p-value) revealed groups of genes repressed and activated by the different manipulations.
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Project description:The zinc finger transcription factor growth-factor-independent-1 (Gfi1) has been involved in various cellular differentiation processes. Gfi1 acts as a transcriptional repressor and splicing control factor upon binding to cognate binding sites in regulatory elements of its target genes. Here, we report that Gfi1-deficient mice develop autoimmunity. Gfi1-deficient peripheral B-cells show a hyperproliferative phenotype, leading to expansion of plasma cells, increased levels of nuclear autoantibodies, and immunoglobulin deposition in brain and kidneys. Dysregulation of multiple transcription factors and cell-cycle control elements may contribute to B-cell dependent autoimmunity. Gfi1 thus emerges as a novel master-regulator restricting autoimmunity. Experiment Overall Design: Splenic B220+CD19+ CD138- B cells of 4 week old Gfi1+/+ and Gfi1-/- mice were isolated and RNA was extracted from one sample per group and microarray analysis was performed.
2008-10-25 | E-GEOD-12545 | biostudies-arrayexpress
Project description:GFI1 is a transcriptional repressor protein that plays an essential role in HSCs development, lymphoid and myeloid differentiation and Acute Myeloid Leukaemic (AML) pathogenesis. Low expression levels of GFI1 is associated with a poor prognosis in AML development. In addition, a single nucleotide polymorphism (SNP) variant of GFI1 results in the generation of GFI1 protein with asparagine (N) instead of serine (S) at the 36th amino acid position, known as GFI136N. Expression of the GFI1-36N allele leads as well to poor prognosis and promotes AML development. In this study, we demonstrated with the help of RNAseq transcriptomic analysis that the presence of GFI1-36N is associated with increased frequency of chromosomal aberrations and mutational burden in murine and human AML cells. In particular, GFI1-36N modulates DNA repair pathways, O6-methylguanine-DNA-methyltransferase (MGMT)-mediated repair and homologous recombination repair (HR). Mechanistically, GFI1-36N exhibits impaired binding to Ndrg1 promoter element compared to GFI1-36S (wild type), causing decreased NDRG1 levels, consequently leading to suppression of MGMT expression, imprinted at the transcriptome and proteome, thus leaving the AML cells vulnerable to DNA damaging agents. Furthermore, we showed that a low expression level of GFI1 in leukemic cells is associated with high OXPHOS and enhanced glutamine metabolism. However, we hypothesise that the observed metabolic phenotype is mediated through FOXO1 protein. RNAseq transcriptomic analysis revealed higher Foxo1 mRNA expression levels with lower GFI1 expression, providing the first hint of Foxo1 as a potential target gene of GFI1 protein. The mRNA and protein levels of high Foxo1 with reduced GFI1 expression was confirmed by RT-PCR and western blot, respectively. In addition, CHIPseq and ATACseq analysis further proved that Foxo1 is a potential target gene of GFI1. In summary, we show that GFI1 plays a role during DNA repair and metabolism and thus provides critical insights into a novel therapeutic option for AML patients carrying the GFI1-36N variant or having a low expression level of GFI1.
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Project description:Genome-wide identification of genes directly regualted by GFI1 and IKAROS in CCRF-CEM cells
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Project description:GFI1 is a transcriptional repressor protein that represses the transcription by mediating chromatin modifications such as histone demethylation, methylation and deacetylation of target genes. The genes with significant open chromatin configuration in the promoter and enhancer regions of GFI1-KI and GFI1-KD mice are identified in this study. This aids in the identification of unique additional genes that might be GFI1 protein's potential targets. We showed a significant open chromatin configuration of Foxo1 promoter and enhancer regions with reduced GFI1 expression. This gives additional support for hypothesising FOXO1 as a target gene of GFI1, along with the data from CHIPseq and RNAseq analysis.
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Project description:Innate type-2 lymphoid cells (ILC2s) function in immune responses against helminth parasites and are implicated in allergic inflammation and asthma. ILC2s are activated by the epithelial-derived cytokines IL-33 and IL-25 and are major sources of the type-2 cytokines IL-5 and IL-13. We show that the transcription factor Gfi1 promotes the generation of ILC2s and controls their responsiveness during Nippostrongylus brasiliensis infection as well as IL-33- or IL-25-instigated inflammation. Gfi1 directly activates Il1rl1, which encodes the IL-33 receptor. IL- 33 signaling upregulates Gfi1, thereby constituting a positive feedback loop that enables rapid and robust expansion of ILC2s in response to IL-33 signaling. Loss of Gfi1 in activated ILC2s results in an unusual effector state involving derepression of the IL-17 inflammatory program and co-expression of IL-13 with IL-17. ChIPseq reveals key Gfi1 targeted genes that are activated or repressed to maintain ILC2 identity. We propose that Gfi1 functions as a shared determinant within innate and adaptive immune cells to specify type-2 responses, while actively repressing the IL-17 effector state. ILC2s (~3 x 10^7 cells) were sorted from the MLN of IL-25-treated mice. Chromatin fragments bound by Gfi1 were subject to ChIP using Gfi1 antibodies and followed by high-throughput sequencing.
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Project description:The zinc finger transcription factor growth-factor-independent-1 (Gfi1) has been involved in various cellular differentiation processes. Gfi1 acts as a transcriptional repressor and splicing control factor upon binding to cognate binding sites in regulatory elements of its target genes. Here, we report that Gfi1-deficient mice develop autoimmunity. Gfi1-deficient peripheral B-cells show a hyperproliferative phenotype, leading to expansion of plasma cells, increased levels of nuclear autoantibodies, and immunoglobulin deposition in brain and kidneys. Dysregulation of multiple transcription factors and cell-cycle control elements may contribute to B-cell dependent autoimmunity. Gfi1 thus emerges as a novel master-regulator restricting autoimmunity.
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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.
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