Transcriptome sequencing of E14.5 fetal liver erythroblast stage 1 cells in WT and LDB1 cKO mice
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PROVIDER: PRJNA1040743 | ENA |
REPOSITORIES: ENA
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Project description:This study investigated the role of LDB1 in early erythroid development by comparing gene expression patterns between WT and LDB1 cKO embryo. These data may provide better knowledge about the exact mechanisms underlying the role of LDB1 in erythropoiesis at distinct differentiation stage.
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Project description:The aim of this experiment was to investigate the role of KLF3 in regulating gene expression at different stages throughout the erythroid maturation process. Affymetrix microarrays were performed on fetal liver cells (both TER119- progenitor cells and TER119+ erythroblast cells) from E14.5 wildtype and Klf3 KO mice. Four wildtype TER119- replicates, four Klf3 KO TER119- replicates, four wildtype TER119+ replicates, three Klf3 KO TER119+ replicates. All are from E14.5 fetal liver.
2012-02-07 | E-GEOD-35592 | biostudies-arrayexpress
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Project description:The monoallelic expression of olfactory receptor (OR) genes is governed by a large number of intergenic enhancer elements that are located in intergenic regions of OR gene clusters. In mature olfactory sensory neurons (OSNs), multiple OR enhancers colocalize in an interchromosomal enhancer hub together with the active OR allele. Here we show that in OSNs OR enhancers are bound by Ldb1, but not general purpose mediators of nuclear architecture (CTCF or the cohesin complex subunit Rad21). Conditional deletion of Ldb1 in OSNs results in the dissolution of long range and interchromosomal contacts between OR Enhancers and in pervasive reductions in OR gene expression.
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Project description:Chromatin organization is a pivotal factor in stem cell pluripotency and differentiation. However, despite considerable study, the role of enhancer looping protein LDB1 in these processes has not been explored. Here, we generated Ldb1(-/-) embryonic stem cells (ESC) using CRISPR/Cas9 editing to understand the significance of LDB1 during development. Ldb1(-/-) ESC exhibited a reduction in key stem cell factors SOX2 and KLF4. Embryoid bodies (EB) derived from Ldb1(-/-) ESC displayed reduced expression of lineage-specific markers and impaired ability to undergo terminal differentiation to erythroblasts. Transcriptome analysis revealed differential gene expression between WT and Ldb1(-/-) ESC and EB but altered gene expression was most pronounced after differentiation to erythroblasts. The Lin28-mediated stem cell self-renewal pathway was dysregulated in Ldb1(-/-) cells. Our data reveal that LDB1 occupies super enhancers of pluripotency genes in ESC together with pluripotency factors. LDB1 loss resulted in a global decrease in chromatin accessibility in ESC and EB. Conditional LDB1-deficient mice showed reduced hematopoietic stem cell markers on bone marrow cells, and dysregulation of the Lin28/Let-7/Hmga2 pathway. We conclude LDB1 function is critical for ESC and EB development and becomes progressively more important during differentiation to erythroblasts.
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Project description:Chromatin organization is a pivotal factor in stem cell pluripotency and differentiation. However, despite considerable study, the role of enhancer looping protein LDB1 in these processes has not been explored. Here, we generated Ldb1(-/-) embryonic stem cells (ESC) using CRISPR/Cas9 editing to understand the significance of LDB1 during development. Ldb1(-/-) ESC exhibited a reduction in key stem cell factors SOX2 and KLF4. Embryoid bodies (EB) derived from Ldb1(-/-) ESC displayed reduced expression of lineage-specific markers and impaired ability to undergo terminal differentiation to erythroblasts. Transcriptome analysis revealed differential gene expression between WT and Ldb1(-/-) ESC and EB but altered gene expression was most pronounced after differentiation to erythroblasts. The Lin28-mediated stem cell self-renewal pathway was dysregulated in Ldb1(-/-) cells. Our data reveal that LDB1 occupies super enhancers of pluripotency genes in ESC together with pluripotency factors. LDB1 loss resulted in a global decrease in chromatin accessibility in ESC and EB. Conditional LDB1-deficient mice showed reduced hematopoietic stem cell markers on bone marrow cells, and dysregulation of the Lin28/Let-7/Hmga2 pathway. We conclude LDB1 function is critical for ESC and EB development and becomes progressively more important during differentiation to erythroblasts.
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Project description:Chromatin organization is a pivotal factor in stem cell pluripotency and differentiation. However, despite considerable study, the role of enhancer looping protein LDB1 in these processes has not been explored. Here, we generated Ldb1(-/-) embryonic stem cells (ESC) using CRISPR/Cas9 editing to understand the significance of LDB1 during development. Ldb1(-/-) ESC exhibited a reduction in key stem cell factors SOX2 and KLF4. Embryoid bodies (EB) derived from Ldb1(-/-) ESC displayed reduced expression of lineage-specific markers and impaired ability to undergo terminal differentiation to erythroblasts. Transcriptome analysis revealed differential gene expression between WT and Ldb1(-/-) ESC and EB but altered gene expression was most pronounced after differentiation to erythroblasts. The Lin28-mediated stem cell self-renewal pathway was dysregulated in Ldb1(-/-) cells. Our data reveal that LDB1 occupies super enhancers of pluripotency genes in ESC together with pluripotency factors. LDB1 loss resulted in a global decrease in chromatin accessibility in ESC and EB. Conditional LDB1-deficient mice showed reduced hematopoietic stem cell markers on bone marrow cells, and dysregulation of the Lin28/Let-7/Hmga2 pathway. We conclude LDB1 function is critical for ESC and EB development and becomes progressively more important during differentiation to erythroblasts.
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Project description:LMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here. RNAseq were performed on HSB cell lines to examine their expression patterns
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Project description:LMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here.
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