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Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in murine hematopoietic stem/progenitor cells

ABSTRACT: Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in murine hematopoietic stem/progenitor cells

PROVIDER: PRJNA348759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4427870.fastq.gz	Fastqsanger.gz
	SRR4427880.fastq.gz	Fastqsanger.gz
	SRR4427890.fastq.gz	Fastqsanger.gz
	SRR4427871.fastq.gz	Fastqsanger.gz
	SRR4427891.fastq.gz	Fastqsanger.gz

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Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in murine hematopoietic stem/progenitor cells (ERRBS)

Project description:Recent studies have uncovered that activation-induced cytidine deaminase (AID) and ten-eleven-translocation (TET) family members regulate active DNA demethylation. Genetic alterations of TET2 in various myeloid malignancies and aberrant hematopoietic stem cell (HSC) self-renewal/differentiation in mice with hematopoietic tissue specific loss of Tet2 have been reported, indicating that TET2 is a master regulator of normal and malignant hematopoiesis. Despite a functional link between AID and TET in epigenetic gene regulation, the role of AID loss in normal hematopoiesis and myeloid transformation remains to be investigated. Here, we show that Aid loss in mice leads to expansion of myeloid cells and contraction in erythroid progenitors resulting in pathologic anemia possibly due to dysregulated expression of Cebpa and Gata1, myeloid/erythroid lineage specific transcription factors. Consistent with data in the murine context, silencing of AID skews differentiation towards myelomonocytic lineage in human BM cells. However, in contrast to Tet2, Aid loss does not contribute to enhanced HSC self-renewal or cooperate with Flt3-ITD in myeloid leukemogenesis. Genome-wide transcription and differential methylation analysis uncover critical role of Aid as a key epigenetic regulator. These results indicate that AID and TET2 share common effects on myeloid and erythroid lineage differentiation, and that their role is non-redundant in regulating HSC self-renewal and in myeloid transformation.

2017-10-01 | GSE88842 | GEO

Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in murine hematopoietic stem/progenitor cells (RNA-Seq)

2017-10-01 | GSE88841 | GEO

Aid is a key regulator of myeloid/erythroid differentiation and DNA methylation in murine hematopoietic stem/progenitor cells

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

2017-10-01 | GSE88843 | GEO

Impact on erythroid progenitor type on erythroid differntiation

Project description:Impact on erythroid progenitor type on erythroid differntiation

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CDK6 as key regulator of hematopoietic and leukemic stem cell activation.

Project description:The cyclin-dependent kinases (CDK) CDK6 and CDK4 have redundant functions in regulating cell-cycle progression. We describe a novel role for CDK6 in hematopoietic and leukemic stem cells (HSCs and LSCs) that exceeds its function as cell-cycle regulator. Although hematopoiesis appears regular under steady state conditions Cdk6-/- HSCs do not efficiently repopulate upon competitive transplantation and Cdk6-deficient mice are significantly more susceptible to 5-fluorouracil (5-FU) treatment. We find that activation of HSCs requires CDK6, which interferes with transcription of key regulators including Egr1. The central role of Egr1 is supported by transcriptional profiling of HSCs. The impaired repopulation capacity extends to BCR-ABLp210+ leukemic stem cells. Transplantation with BCR-ABLp210+-infected bone marrow (BM) from Cdk6-/- mice fails to induce disease although recipient mice do harbor LSCs. Egr1 knock-down in cdk6-/- BCR-ABLp210+ LSKs significantly enhances colony formation underlining the importance of the Cdk6-Egr1 axis. Our findings define CDK6 as an important regulator of stem cell activation and as essential component of a transcriptional complex that suppresses Egr1 in HSCs and LSCs. Four-condition experiment, Untreated or polyI:C-treated CDK6-/- cells versus untreated or polyI:C-treated wild-type cells. Biological replicates: 3 untreated replicates, 3 polyI:C-treated replicates.

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Differential gene expression of Epo induced hematopoietic stem/progenitor cell erythroid differentiation with HBBP1 depletion

Project description:This work shows HBBP1 is indispensable for erythropoiesis. HBBP1 was knocked down by two specific shRNAs (shHBBP1-1, shHBBP1-2) during erythroid differentiation induced from cord blood derived hematopoietic progenitor cells. After delivering shRNAs into cells, fewer mature erythroid cells in knock-down cells compared to control cells across all differentiation timings. Differential transcriptome data analysis further revealed the overall inhibition of genes promoting erythroid differentiation.

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RNA-seq transcriptional profiling in human primary fetal and adult CD34+ hematopoietic stem/progenitor cells (HSPCs) erythroid progenitor cells (ProEs)

Project description:Advances in sequencing-based genomic profiling present a new challenge of explaining how changes in DNA/RNA are translated into proteins linking genotypes to phenotypes. The developing erythroid cells require highly coordinated gene expression and metabolism, and serve as a unique model in dissecting regulatory events in development and disease. Here we compare the proteomic and transcriptomic changes in human hematopoietic stem/progenitor cells and lineage-committed erythroid progenitors, and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Two principal mitochondrial factors TFAM and PHB2 are tightly regulated at the protein level and indispensable for mitochondria and erythropoiesis. mTORC1 signaling is progressively enhanced to promote translation of mitochondrial proteins during erythroid specification. Genetic and pharmacological perturbation of mTORC1 or mitochondria impairs erythropoiesis. Our studies suggest a new mechanism for regulation of mitochondrial biogenesis through mTORC1-mediated protein translation, and may have direct relevance to the hematological defects associated with mitochondrial diseases and aging. Transcriptional profiling in human primary fetal and adult CD34+ hematopoietic stem/progenitor cells (HSPCs) erythroid progenitor cells (ProEs) by RNA-seq analysis.

2017-05-15 | E-GEOD-74053 | biostudies-arrayexpress

Erythropoietin guides multipotent hematopoietic progenitor cells toward an erythroid fate.

Project description:The erythroid stress cytokine erythropoietin (Epo) supports the development of committed erythroid progenitors, but its ability to act on upstream, multipotent cells remains to be established. We observe that high systemic levels of Epo reprogram the transcriptomes of multi- and bipotent hematopoietic stem/progenitor cells in vivo. This induces erythroid lineage bias at all lineage bifurcations known to exist between hematopoietic stem cells (HSCs) and committed erythroid progenitors, leading to increased erythroid and decreased myeloid HSC output. Epo, therefore, has a lineage instructive role in vivo, through suppression of non-erythroid fate options, demonstrating the ability of a cytokine to systematically bias successive lineage choices in favor of the generation of a specific cell type.

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SNP analysis AID-low vs AID-high

Project description:SNP analysis AID-low vs AID-high

2009-07-20 | GSE13612 | GEO

RNA-seq transcriptional profiling in human primary fetal and adult CD34+ hematopoietic stem/progenitor cells (HSPCs) erythroid progenitor cells (ProEs)

2017-05-15 | GSE74053 | GEO