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Microarray expression level comparison between WT and KO fetal liver cells

ABSTRACT: The erythroid Krüppel-like factor EKLF/KLF1 is a hematopoietic transcription factor binding to CACCC DNA motif and participating in the regulation of erythroid differentiation. With combined use of microarray-based gene expression profiling and promoter-based ChIP-chip assay of E14.5 fetal liver cells from wild type (WT) and EKLF-knockout (Eklf-/-) mouse embryos, we have identified the pathways and direct target genes activated or repressed by EKLF. This genome-wide study together with molecular/ cellular analysis of mouse erythroleukemic cells (MEL) indicate that among the downstream direct target genes of EKLF is Tal1/Scl. Tal1/Scl encodes another DNA-binding hematopoietic transcription factor TAL1/SCL known to be an Eklf activator and essential for definitive erythroid differentiation. Further identification of the authentic Tall gene promoter in combination with in vivo genomic footprinting approach and DNA reporter assay demonstrate that EKLF activates Tall gene through binding to a specific CACCC motif located in its promoter. These data establish the existence of a previously unknow positive regulatory feedback loop between two DNA-binding hematopoietic transcription factors that sustains the mammalian erythropoiesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE171200 | GEO | 2022/03/31

REPOSITORIES: GEO

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ChIP-Chip data from WT E14.5 fetal liver

Project description:The erythroid Krüppel-like factor EKLF/KLF1 is a hematopoietic transcription factor binding to CACCC DNA motif and participating in the regulation of erythroid differentiation. With combined use of microarray-based gene expression profiling and promoter-based ChIP-chip assay of E14.5 fetal liver cells from wild type (WT) and EKLF-knockout (Eklf-/-) mouse embryos, we have identified the pathways and direct target genes activated or repressed by EKLF. This genome-wide study together with molecular/ cellular analysis of mouse erythroleukemic cells (MEL) indicate that among the downstream direct target genes of EKLF is Tal1/Scl. Tal1/Scl encodes another DNA-binding hematopoietic transcription factor TAL1/SCL known to be an Eklf activator and essential for definitive erythroid differentiation. Further identification of the authentic Tall gene promoter in combination with in vivo genomic footprinting approach and DNA reporter assay demonstrate that EKLF activates Tall gene through binding to a specific CACCC motif located in its promoter. These data establish the existence of a previously unknow positive regulatory feedback loop between two DNA-binding hematopoietic transcription factors that sustains the mammalian erythropoiesis.

2022-03-31 | GSE171201 | GEO

Genome-wide ChIP-Seq reveals a dramatic shift in the binding of the transcription factor erythroid Kruppel-like factor during erythrocyte differentiation

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2013-06-17 | E-GEOD-48020 | biostudies-arrayexpress

Genome-wide maps of Scl/TAL1 in human erythroid cells.

Project description:ChIP-Seq experiments using an Scl/TAL1 antibody were carried out in primary erythroid cells cultured from two individuals of Caucasian origin. ChIP-Seq libraries were prepared from two biological replicates for each individual. ChIP DNA was processed for Illumina High-throughput sequencing according to Illumina protocol. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA from each experiments, we generated a high-resolution map of Scl/TAL1 genomic targets in human erythroid cells. We find that WGATAR and the combinatorial CTG(n9)GATA are the most significant motifs responsible for the chromatin occupancy by Scl/TAL1. In addition, other motifs are also significantly enriched at the Scl/TAL1 targets. Amongst these were binding sites for known TFs (Sp/XKLF, RUNX1, NFE2). We next investigated how many of these targets varied between these two individuals. We find that 0.8% of Scl/TAL1 binding regions differ significantly between the two individuals.

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Genome-wide ChIP-Seq reveals a dramatic shift in the binding of the transcription factor erythroid Kruppel-like factor during erythrocyte differentiation

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SCL and c-Kit controlled gene expression in erythroid progenitor cell line

Project description:SCL/TAL1, a tissue-specific transcription factor of the basic helix-loop-helix (bHLH) family, and c-Kit, a tyrosine kinase receptor, control hematopoietic stem cell survival and quiescence. Here we report that SCL and c-Kit signaling control a common gene expression signature, of which 19 genes are associated with apoptosis. In vivo, SCL levels are limiting for the clonal expansion of Kit+ multipotent and erythroid progenitors. In addition, increased SCL expression specifically enhances the sensitivity of multipotent and megakaryocyte/erythroid progenitors to Steel factor (KIT ligand), whilst a DNA binding mutant antagonizes KIT function and induces apoptosis in progenitors. We conclude that Scl operates downstream of Kit to support the survival of megakaryocyte/erythroid progenitors. Finally, higher SCL expression upregulates Kit in normal bone marrow cells and increases chimerism after bone marrow transplantation, indicating that Scl is also upstream of Kit. We conclude that Scl and Kit establish a positive feedback loop in multipotent and megakaryocyte/erythroid progenitors. c-Kit regulated genes were extrapolated from gene expression profiles of TF-1 erythroid progenitor cells (empty MSCV vector) stimulated with SF (Kit ligand), Epo or GM-CSF. Second, SCL-regulated genes were obtained by expressing a DNA binding-defective SCL mutant (DbSCL) and selecting genes that were differentially expressed in M-oM-^AM-^DbSCL cells versus control cells (MSCV) stimulated with the same cytokines.

2013-07-06 | E-GEOD-48557 | biostudies-arrayexpress

SCL and c-Kit controlled gene expression in erythroid progenitor cell line

2013-07-06 | GSE48557 | GEO

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [RNA-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl and Gata 1 & 2 target genes in ES cell derived day4.75 EB (embryoid body) Tie2+CD31+CD41- endothelial cells

2015-01-01 | E-GEOD-47083 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [expression]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl target genes in ES cell derived day4 EB (embryoid body) Flk+ mesodermal cells

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Differential genomic targeting of the transcription factor TAL1 in alternate hematopoietic lineages

Project description:TAL1/SCL is a master regulator of hematopoiesis whose expression promotes opposite outcomes depending on the cell type - differentiation in the erythroid lineage or oncogenesis in the T-cell lineage. Here we used a combination of ChIP-sequencing and gene expression profiling to compare the function of TAL1 in normal erythroid and leukemic T-cells. Analysis of the genome-wide binding properties of TAL1 in these two hematopoietic lineages revealed new insight into the mechanism by which transcription factors select their binding sites in alternate lineages. Our study shows limited overlap in the TAL1 binding profile between the two cell types with an unexpected preference for ETS and RUNX motifs adjacent to E-boxes in the T-cell lineage. Furthermore we show that TAL1 interacts with RUNX1 and ETS1, and that these transcription factors are critically required to target TAL1 to genes that modulate T-cell differentiation. Thus, our findings highlight a critical role of the cellular environment in modulating transcription factor binding, and provide insight into the mechanism by which TAL1 inhibits differentiation leading to oncogenesis in the T-cell lineage. Examine TAL1/SCL binding sites in two different cell lineages (i.e. primary human pro-erythroblasts and the Jurkat T-ALL cell line). These records represent the ChIP-seq part of the study. The gene expresssion part is available at GSE20546.

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