TAL1 knock down in human erythroid progenitors
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE20545 | GEO | 2010/12/14
SECONDARY ACCESSION(S): PRJNA129859
REPOSITORIES: GEO
Similar Datasets
Project description:We used microarray profiling in erythroid cells to uncover TAL1 dependent genes in a hematopoietic differentiation context. Differentiated ex vivo hematopoietic multipotential progenitors isolated from adult peripheral blood. The knockdown of TAL1 (KD) was induced in pro-erythroblasts (Days 8 and 9 of differentiation) using lentivirus-delivered shRNA. A scramble (scr) shRNA sequence was used as a negative control.
2010-12-14 | E-GEOD-20545 | biostudies-arrayexpress
Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context.
2010-12-14 | GSE20544 | GEO
Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context. Clonal Jurkat lines expressing a Doxycycline (Dox) -inducible shRNA against TAL1 coding sequence were generated. A clone in which Dox treatment led to 80% decrease of TAL1 mRNA was chosen.
2010-12-14 | E-GEOD-20544 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE20544: TAL1 knock down in Jurkat cells GSE20545: TAL1 knock down in human erythroid progenitors Refer to individual Series
2010-12-14 | E-GEOD-20546 | biostudies-arrayexpress
Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.
2021-09-09 | PXD018052 | Pride
Project description:We report the occupancy of GATA1 and TAL1, two erythroid transcription factors, and H3K27ac histone modification in human erythroid precursors.
2017-01-10 | GSE93372 | GEO
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.
2014-11-08 | GSE42390 | GEO
Project description:Aberrant activation of the TAL1 oncogene is associated with up to 60% of T-ALL patients and is involved in CTCF mediated genome organization within the TAL1 locus, suggesting the importance of the CTCF boundary in the molecular pathogenesis of T-ALL. Here, we show that deletion of CTCF binding site (CBS) or alternation of CTCF boundary orientation alters expression of the TAL1 oncogene in a cell context dependent manner. Deletion of the CTCF binding site located at -31 Kb upstream of TAL1 (-31CBS) reduces chromatin accessibility in the +51 enhancer and the TAL1 promoter I, and blocks long-range interaction between the +51 erythroid enhancer and TAL1 promoter 1b that inhibits expression of TAL1 in erythroid cells, but not in T-ALL cells. However, in the TAL1 expressed T-ALL primary patient samples or cell line, the T-ALL prone TAL1 promoter IV specifically interacts with the +19 stem cell enhancer that is located 19 kb downstream of the TAL1 promoter and required for TAL1 transcription in the hematopoietic stem cell (HSC) stage. Inversion of -31CBS orientation, but not deletion of -31CBS, alters chromatin accessibility, enhancer/promoter histone modifications, CTCF-mediated topological associated domain (TAD), and enhancer/promoter interaction in the TAL1 locus leading to inhibition of TAL1 oncogene expression and TAL1-driven T cell leukemogenesis. Thus, our data reveal that the TAL1 +19 stem cell enhancer acts not only as stem cell enhancer, but also as a leukemia specific enhancer to activate the TAL1 oncogene in T-ALL. Manipulation of CTCF defined chromatin boundary can alter TAL1 TAD and oncogenic transcription networks in leukemogenesis.
2020-04-06 | GSE135320 | GEO
Project description:Endothelial colony-forming cells (ECFCs) have been reported as promising cells for regenerative medicine thanks to their angiorepair properties. Transcription factors are primary determinants of the functional capacity of the cells and TAL1 has been shown as a critical regulator of endothelial lineage in both development and adult life. However, only few (three) TAL1 targets have been identified so far in mouse and human endothelial cells. This microarray experiment, where TAL1 expression was knocked-down, was designed to identify TAL1-dependent genes in primary human endothelial stem/progenitor cells.
2014-05-06 | GSE44444 | GEO
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.
2010-10-30 | E-GEOD-25000 | biostudies-arrayexpress