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

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

PROVIDER: PRJNA826497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18745500_1.fastq.gz	Fastqsanger.gz
	SRR18745500_2.fastq.gz	Fastqsanger.gz
	SRR18745501_1.fastq.gz	Fastqsanger.gz
	SRR18745501_2.fastq.gz	Fastqsanger.gz
	SRR18745502_1.fastq.gz	Fastqsanger.gz

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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- 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 [ikaros]

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

| PRJNA887794 | 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 hematopoietic differentiation in zebrafish [it325]

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 | GSE214953 | GEO

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

2022-10-08 | GSE214952 | GEO

Stage-specific 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. Four zinc fingers constitute its DNA binding domain and two zinc fingers are present in the C-terminal protein interaction module. 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. 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. Both mutations 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.

| S-EPMC9741631 | biostudies-literature

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-10-07 | GSE214955 | GEO

Zebrafish periderm at 4-somite stage

Project description:Zebrafish periderm at 4-somite stage

| PRJNA589023 | ENA

Efficacy of retinoids in IKZF1-mutated BCR-ABL1 acute lymphoblastic leukemia

Project description:Alterations of IKZF1, encoding the lymphoid transcription factor IKAROS, are a hallmark of high risk acute lymphoblastic leukemia (ALL), however the role of IKZF1 alterations in ALL pathogenesis is poorly understood. Here we show that in mouse models of BCR-ABL1 leukemia, Ikzf1 and Arf alterations synergistically promote the development of an aggressive lymphoid leukemia. Ikzf1 alterations were associated with acquisition of stem cell-like features, including self-renewal and increased bone marrow stromal adhesion. Rexinoid receptor agonists reversed this phenotype, in part by inducing expression of IKZF1, resulting in abrogation of adhesion and self-renewal, cell cycle arrest and attenuation of proliferation without direct cytotoxicity. Retinoids potentiated the activity of dasatinib in mouse and human BCR-ABL1 ALL, providing a new therapeutic option in IKZF1-mutated ALL. Significance: The outcome of therapy for high-risk acute lymphoblastic leukemia remains suboptimal despite contemporary chemotherapy and the advent of targeted therapeutic approaches. Recent genomic studies have identified deletions or mutations of IKZF1 as a hallmark of high-risk ALL, but an understanding of how IKZF1 alteration contribute to leukemia development are lacking. Here we show that IKZF1 alterations drive lymphoid lineage, a stem cell-like phenotype, abnormal bone marrow adhesion, and poor responsiveness to tyrosine kinase inhibitor (TKI) therapy. Using a high-content screen, we show that retinoids reverse this phenotype in part by inducing expression of wild type IKZF1, and increase responsiveness to TKIs. These findings provide new insight into the pathogenesis of high-risk ALL and potential new therapeutic approaches. Pre-B mRNA profiles of p185 MIG and IK6 cells, DMSO or drug treated, in 3 or 4 replicates, using Illumina HiSeq 2500.

2015-09-04 | E-GEOD-68391 | biostudies-arrayexpress

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