BCL11A is required for normal erythropoiesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1195589 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31642620_1.fastq.gz | Fastqsanger.gz | |||
| SRR31642620_2.fastq.gz | Fastqsanger.gz | |||
| SRR31642621_1.fastq.gz | Fastqsanger.gz | |||
| SRR31642621_2.fastq.gz | Fastqsanger.gz | |||
| SRR31642622_1.fastq.gz | Fastqsanger.gz |
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Project description:BCL11A is required for normal erythropoiesis [RNA-seq_Sorted]
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Project description:BCL11A is required for normal erythropoiesis [ATAC-seq]
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Project description:BCL11A is required for normal erythropoiesis [CUT&Run]
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Project description:Genetic depletion of the transcriptional repressor BCL11A in red blood cell precursors alleviates b-hemoglobinopathies by inducing the fetal g-globin genes. However, several additional erythroid genes are regulated by BCL11A and the effects of its deficiency on erythropoiesis are insufficiently described. We discovered that Cas9 disruption of the BCL11A intron 2 erythroid enhancer in CD34+ hematopoietic stem and progenitor cells (HSPCs) according to a clinically approved strategy caused impaired expansion and increased apoptosis of erythroid precursors in vitro and in vivo. Mutant colony-forming unit erythroid (CFU-e), proerythroblasts, and basophilic erythroblasts exhibited dysregulation of 94 genes (> 2-fold change, FDR < 0.05). 25 of which are likely direct targets of BCL11A. Differentially expressed genes were associated with numerous biological pathways that impact cell expansion and survival. Our findings show that BCL11A regulates additional aspects of erythropoiesis beyond g-globin gene repression.
2024-12-09 | GSE283794 | GEO
Project description:Genetic depletion of the transcriptional repressor BCL11A in red blood cell precursors alleviates b-hemoglobinopathies by inducing the fetal g-globin genes. However, several additional erythroid genes are regulated by BCL11A and the effects of its deficiency on erythropoiesis are insufficiently described. We discovered that Cas9 disruption of the BCL11A intron 2 erythroid enhancer in CD34+ hematopoietic stem and progenitor cells (HSPCs) according to a clinically approved strategy caused impaired expansion and increased apoptosis of erythroid precursors in vitro and in vivo. Mutant colony-forming unit erythroid (CFU-e), proerythroblasts, and basophilic erythroblasts exhibited dysregulation of 94 genes (> 2-fold change, FDR < 0.05). 25 of which are likely direct targets of BCL11A. Differentially expressed genes were associated with numerous biological pathways that impact cell expansion and survival. Our findings show that BCL11A regulates additional aspects of erythropoiesis beyond g-globin gene repression.
2024-12-09 | GSE283793 | GEO
Project description:Genetic depletion of the transcriptional repressor BCL11A in red blood cell precursors alleviates b-hemoglobinopathies by inducing the fetal g-globin genes. However, several additional erythroid genes are regulated by BCL11A and the effects of its deficiency on erythropoiesis are insufficiently described. We discovered that Cas9 disruption of the BCL11A intron 2 erythroid enhancer in CD34+ hematopoietic stem and progenitor cells (HSPCs) according to a clinically approved strategy caused impaired expansion and increased apoptosis of erythroid precursors in vitro and in vivo. Mutant colony-forming unit erythroid (CFU-e), proerythroblasts, and basophilic erythroblasts exhibited dysregulation of 94 genes (> 2-fold change, FDR < 0.05). 25 of which are likely direct targets of BCL11A. Differentially expressed genes were associated with numerous biological pathways that impact cell expansion and survival. Our findings show that BCL11A regulates additional aspects of erythropoiesis beyond g-globin gene repression.
2024-12-09 | GSE283796 | GEO
Project description:Genetic depletion of the transcriptional repressor BCL11A in red blood cell precursors alleviates b-hemoglobinopathies by inducing the fetal g-globin genes. However, several additional erythroid genes are regulated by BCL11A and the effects of its deficiency on erythropoiesis are insufficiently described. We discovered that Cas9 disruption of the BCL11A intron 2 erythroid enhancer in CD34+ hematopoietic stem and progenitor cells (HSPCs) according to a clinically approved strategy caused impaired expansion and increased apoptosis of erythroid precursors in vitro and in vivo. Mutant colony-forming unit erythroid (CFU-e), proerythroblasts, and basophilic erythroblasts exhibited dysregulation of 94 genes (> 2-fold change, FDR < 0.05). 25 of which are likely direct targets of BCL11A. Differentially expressed genes were associated with numerous biological pathways that impact cell expansion and survival. Our findings show that BCL11A regulates additional aspects of erythropoiesis beyond g-globin gene repression.
2024-12-09 | GSE283795 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-12-08 | GSE283797 | GEO
Project description:Bcl11a is a transcription factor known to regulate lymphoid and erythroid development. Recent bioinformatic analysis of global gene expression patterns has suggested a role for Bcl11a in the development of dendritic cell (DC) lineages. We tested this hypothesis by analyzing the development of DC and other lineages in Bcl11a(-/-) mice. We show that Bcl11a is required for expression of IL-7 receptor (IL-7R) and Flt3 in early hematopoietic progenitor cells. The loss of IL-7R(+) common lymphoid progenitors accounts for previously described lymphoid defects in Bcl11a(-/-) mice. In addition, we found severely decreased numbers of plasmacytoid dendritic cells (pDCs) in Bcl11a(-/-) fetal livers and in the bone marrow of Bcl11a(-/-) fetal liver chimeras. Moreover, Bcl11a(-/-) cells show severely impaired in vitro development of Flt3L-derived pDCs and classical DCs (cDCs). In contrast, we found normal in vitro development of DCs from Bcl11a(-/-) fetal liver cells treated with GM-CSF. These results suggest that the persistent cDC development observed in Bcl11a(-/-) fetal liver chimeras reflects derivation from a Bcl11a- and Flt3-independent pathway in vivo. We compared global gene expression by microarray for donor-derived wild-type and Bcl11a(-/-) populations isolated from chimeric bone marrow to identify Bcl11a target genes that explain its role in hematopoietic progenitors. GMP and MPP populations were sorted from fetal liver chimeras and pooled by donor genotype. RNA was isolated using an RNAqueous-Micro Kit (Ambion) and submitted for amplification, labeling and hybridization. Expression values were analyzed after RMA quantile normalization using ArrayStar software (DNASTAR).
2013-05-06 | E-GEOD-46270 | biostudies-arrayexpress