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Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [ikaros]

ABSTRACT: Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [ikaros]

PROVIDER: PRJNA887794 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21831645_1.fastq.gz	Fastqsanger.gz
	SRR21831645_2.fastq.gz	Fastqsanger.gz
	SRR21831646_1.fastq.gz	Fastqsanger.gz
	SRR21831646_2.fastq.gz	Fastqsanger.gz
	SRR21831647_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [ikaros]

Project description:The characterisation of two zebrafish ikzf1 mutant lines missing the two C-terminal zinc fingers only and both part of the DNA binding domain plus the C-terminal zinc fingers respectively gives insight into the specific roles of these elements during zebrafish hematopoiesis

2022-10-08 | GSE214952 | GEO

Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish

Project description:Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish

| PRJNA887792 | ENA

Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [it325]

Project description:Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [it325]

| PRJNA887793 | ENA

Stage- and cell type-specific requirements of ikzf1 during haematopoietic differentiation in zebrafish

Project description:Stage- and cell type-specific requirements of ikzf1 during haematopoietic differentiation in zebrafish

| PRJNA826497 | ENA

Stage- and cell type-specific requirements of ikzf1 during hematopoietic differentiation in zebrafish [it325]

2022-10-08 | GSE214953 | GEO

Stage- and cell type-specific requirements of ikzf1 during haematopoietic differentiation in zebrafish

Project description:The zinc finger transcription factor Ikaros1 (Ikzf1) is required for lymphoid development in mammals. It is characterized by the presence of four zinc fingers in its DNA binding domain and two zinc fingers in the C-terminal protein interaction module. Here, we describe the phenotypes of zebrafish homozygous for two distinct mutant ikzf1 alleles. The IT325 variant lacks the C-terminal two zinc fingers, whereas the fr105 variant retains only the first zinc finger of the DNA binding domain. Our results indicate that an intact ikzf1 gene is required for larval T cell development, whereas low levels of adult lymphoid development recover in the mutants. By contrast, the mutants exhibit a signature of increased myelopoiesis at larval and adult stages. Of note, both mutants stimulate erythroid differentiation in larvae, indicating that the C-terminal zinc fingers negatively regulate the extent of red blood cell production. An unexpected differential effect of the two mutants on adult erythropoiesis suggests a direct requirement of an intact DNA binding domain for entry of progenitors into the red blood cell lineage. Collectively, our results reinforce the biological differences between larval and adult haematopoiesis, indicate a stage-specific function of ikzf1 in regulating the hierarchical bifurcations of differentiation, and assign distinct functions to the DNA binding domain and the C-terminal zinc fingers.

2022-12-09 | GSE200756 | 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

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

2014-02-09 | GSE53595 | 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 [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

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