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Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment

ABSTRACT: Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment

PROVIDER: PRJNA705610 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13811411_1.fastq.gz	Fastqsanger.gz
	SRR13811411_2.fastq.gz	Fastqsanger.gz
	SRR13811412_1.fastq.gz	Fastqsanger.gz
	SRR13811412_2.fastq.gz	Fastqsanger.gz
	SRR13811413_1.fastq.gz	Fastqsanger.gz

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Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment

Project description:We present InTAC-seq, a method for simultaneous quantification of genome-wide open chromatin and intracellular protein abundance in fixed cells. Using InTAC we directly observe variation in chromatin accessibility and transcription factor motif occupancy driven by differences in transcription factor protein abundance. By purifying bone marrow progenitor cells based on GATA1 protein expression, we establish its role in both functional and epigenetic restriction of erythroid cell identity in human hematopoiesis.

2022-03-10 | GSE167934 | GEO

Integrating transcription-factor abundance with chromatin accessibility in human erythroid lineage commitment.

Project description:Master transcription factors (TFs) directly regulate present and future cell states by binding DNA regulatory elements and driving gene-expression programs. Their abundance influences epigenetic priming to different cell fates at the chromatin level, especially in the context of differentiation. In order to link TF protein abundance to changes in TF motif accessibility and open chromatin, we developed InTAC-seq, a method for simultaneous quantification of genome-wide chromatin accessibility and intracellular protein abundance in fixed cells. Our method produces high-quality data and is a cost-effective alternative to single-cell techniques. We showcase our method by purifying bone marrow (BM) progenitor cells based on GATA-1 protein levels and establish high GATA-1-expressing BM cells as both epigenetically and functionally similar to erythroid-committed progenitors.

| S-EPMC9017139 | biostudies-literature

Inferring rules of lineage commitment in haematopoiesis

Project description:Fractionation of EML cells isolated based on surface expression of immunophenotypic markers reveals the existence of a subpopulation that has undergone spontaneous commitment to an erythroid fate. Uncommitted fractions were compared to committed cells, derived from both spontaneous (EryCP) and cytokine-driven (Ediff) commitment. EML cells were separated by flow cytometry based on their expression of the markers Sca1, CD34 and cKit as described.

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Inferring rules of lineage commitment in haematopoiesis

2012-02-14 | GSE34605 | GEO

Carfilzomib-induced reticulocytosis in patients with multiple myeloma is caused by impaired terminal erythroid maturation

Project description:Proteasome inhibition constitutes a cornerstone of multiple myeloma (MM) treatment, with bortezomib, carfilzomib and ixazomib approved for clinical use. We observed a consistent and highly significant increase in the reticulocyte count during treatment with carfilzomib-based regimens in patients with relapsed MM, an observation not made in a matched cohort of bortezomib-treated patients. As this increased reticulocytosis was neither associated with elevated hemoglobin levels nor with hemolysis, we subsequently performed in vitro experiments to unravel the underlying mechanisms of this clinical observation. While carfilzomib did not affect erythroid differentiation of CD34+ hematopoietic progenitor cells, both continuous and pulse exposure to carfilzomib significantly impaired terminal maturation of purified primary reticulocytes towards erythrocytes. These results indicate that carfilzomib significantly impairs terminal erythroid maturation, independent of erythroid commitment, expansion or differentiation. Our results report the first pharmacologically induced delay in erythroid maturation as a mechanism for carfilzomib-induced reticulocytosis in MM patients. Quantitative proteomics using LC-MS/MS were performed to assess whether carfilzomib treatment alters the protein composition of reticulocytes

2020-02-20 | PXD014353 | Pride

The histone methyltransferase Setd8 alters the chromatin landscape and regulates the expression of key transcription factorsduring erythroid differentiation

Project description:SETD8 is the sole methyltransferase capable of mono-methylating histone H4, lysine 20. SETD8 is highly expressed in erythroid cells and erythroid deletion of Setd8 is embryonic lethal by embryonic day 11.5 (E11.5) due to profound anemia, suggesting it has an erythroid-specific function. To gain insights into the function of SETD8 during erythroid differentiation, we performed ATAC-seq on sorted populations of E10.5 Setd8 null and control erythroblasts. Accessibility profiles were integrated with expression changes and a mark of heterochromatin (H3K27me3) performed in wild type E10.5 erythroblasts to further understand the role of SETD8 in erythropoiesis. Data integration identified regions of greater chromatin accessibility in Setd8 null cells that co-located with H3K27me3 in wild type E10.5 erythroblasts suggesting that these regions, and their associated genes, are repressed during normal erythropoiesis. Pathway analysis of genes identified through data integration revealed stemness-related pathways. Among those genes were multiple transcriptional regulators active in multipotent progenitors but repressed during erythroid differentiation including Hhex, Hlx, and Gata2. Consistent with a role for SETD8 in erythroid specification, SETD8 expression is upregulated upon erythroid commitment, and Setd8 disruption impairs erythroid colony forming ability. Taken together, our results suggest that Setd8 is important for the establishment of appropriate patterns of gene expression during erythroid differentiation.

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Ribosome Levels Selectively Regulate Translation and Lineage Commitment in Human Hematopoiesis

Project description:Khajuria RK, Munschauer M, Ulirsch JC, Fiorini C, Leif S. Ludwig LS, McFarland SK, Abdulhay NJ, Specht H, Keshishian H, Mani DR, Jovanovic M, Ellis SR, Fulco CP, Engreitz JM, Schütz S, Lian J, Gripp KW,Weinberg OK, Pinkus GS, Gehrke L, Regev A, Lander ES, Gazda HT, Lee WY, Panse VG, Carr SA, Sankaran VG. Cell 2018, 173, 90–103. https://doi.org/10.1016/j.cell.2018.02.036. Blood cell formation is classically thought to occur through a hierarchical differentiation process, although recent studies have shown that lineage commitment may occur earlier in hematopoietic stem and progenitor cells (HSPCs). The relevance to human blood diseases and the underlying regulation of these refined models remain poorly understood. By studying a genetic blood disorder, Diamond-Blackfan anemia (DBA), where the majority of mutations affect ribosomal proteins and the erythroid lineage is selectively perturbed, we are able to gain mechanistic insight into how lineage commitment is programmed normally and disrupted in disease. We show that in DBA, the pool of available ribosomes is limited, while ribosome composition remains constant. Surprisingly, this global reduction in ribosome levels more profoundly alters translation of a select subset of transcripts. We show how the reduced translation of select transcripts in HSPCs can impair erythroid lineage commitment, illuminating a regulatory role for ribosome levels in cellular differentiation.

2016-10-24 | MSV000080283 | MassIVE

A protein phosphatase network controls the temporal and spatial dynamics of differentiation commitment in human epidermis

Project description:Epidermal homeostasis depends on a balance between stem cell renewal and terminal differentiation. The transition between the two cell states,termed commitment, is poorly understood. Here we characterise commitment by integrating transcriptomic and proteomic data from disaggregated primary human keratinocytes held in suspension to induce differentiation. Cell detachment induces several protein phosphatases, five of which - DUSP6, PPTC7, PTPN1, PTPN13 and PPP3CA – promote differentiation by negatively regulating ERK MAPK and positively regulating AP1 transcription factors. Conversely, DUSP10 expression antagonises commitment. The phosphatases form a dynamic network of transient positive and negative interactions that change over time, with DUSP6 predominating at commitment. Boolean network modelling identifies a mandatory switch between two stable states (stem and differentiated) via an unstable (committed) state. Phosphatase expression is also spatially regulated in vivo and in vitro. We conclude that an auto-regulatory phosphatase network maintains epidermal homeostasis by controlling the onset and duration of commitment.

2017-10-18 | PXD003281 | Pride

Genome-wide maps of chromatin accessibility in C57bl\6 mouse erythroid cells.

Project description:Genome-wide identification of active regions in the mouse erythroid genome using DNase-seq. DNAse-seq was performed in C57bl\6 mouse erythroid Ter119+ cells.

2013-11-11 | E-GEOD-49458 | biostudies-arrayexpress

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2022-08-14 | GSE189474 | GEO

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