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O-GlcNAc Homeostasis Controls Cell Fate Decisions During Hematopoiesis

ABSTRACT: O-GlcNAc Homeostasis Controls Cell Fate Decisions During Hematopoiesis

PROVIDER: PRJNA503593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8156060_1.fastq.gz	Fastqsanger.gz
	SRR8156060_2.fastq.gz	Fastqsanger.gz
	SRR8156061_1.fastq.gz	Fastqsanger.gz
	SRR8156061_2.fastq.gz	Fastqsanger.gz
	SRR8156062_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

O-GlcNAc Homeostasis Controls Cell Fate Decisions During Hematopoiesis

Project description:The addition of O-GlcNAc (a single β-D-N-acetylglucosamine sugar at serine and threonine residues) by O-GlcNAc transferase (OGT) and removal by O-GlcNAcase (OGA) maintains homeostatic levels of O-GlcNAc. We investigated the role of OGlcNAc homeostasis in hematopoiesis utilizing G1E-ER4 cells carrying a GATA-1 transcription factor fused to the estrogen receptor (GATA-1ER) that undergo erythropoiesis following the addition of β-estradiol (E2) and myeloid leukemia cells that differentiate into neutrophils in the presence of all-trans retinoic acid. During G1E-ER4 differentiation, a decrease in overall O-GlcNAc levels and an increase in GATA-1 interactions with OGT and OGA were observed. Transcriptome analysis on G1E-ER4 cells differentiated in the presence of Thiamet-G (TMG), an OGA inhibitor, identified expression changes in 433 GATA-1 target genes. Chromatin immunoprecipitation demonstrated that the occupancy of GATA-1, OGT, and OGA at Laptm5 gene GATA site was decreased with TMG. Myeloid leukemia cells showed a decline in O-GlcNAc levels during differentiation and TMG reduced the expression of genes involved in differentiation. Sustained treatment with TMG in G1E-ER4 cells prior to differentiation caused a reduction of hemoglobin positive cells during differentiation. Our results show that alterations in O-GlcNAc homeostasis disrupt transcriptional programs causing differentiation errors suggesting a vital role of O-GlcNAcylation in control of cell fate.

2018-11-06 | GSE122104 | GEO

<i>O</i>-GlcNAc homeostasis contributes to cell fate decisions during hematopoiesis.

Project description:The addition of a single β-d-GlcNAc sugar (O-GlcNAc) by O-GlcNAc-transferase (OGT) and O-GlcNAc removal by O-GlcNAcase (OGA) maintain homeostatic O-GlcNAc levels on cellular proteins. Changes in protein O-GlcNAcylation regulate cellular differentiation and cell fate decisions, but how these changes affect erythropoiesis, an essential process in blood cell formation, remains unclear. Here, we investigated the role of O-GlcNAcylation in erythropoiesis by using G1E-ER4 cells, which carry the erythroid-specific transcription factor GATA-binding protein 1 (GATA-1) fused to the estrogen receptor (GATA-1-ER) and therefore undergo erythropoiesis after β-estradiol (E2) addition. We observed that during G1E-ER4 differentiation, overall O-GlcNAc levels decrease, and physical interactions of GATA-1 with both OGT and OGA increase. RNA-Seq-based transcriptome analysis of G1E-ER4 cells differentiated in the presence of the OGA inhibitor Thiamet-G (TMG) revealed changes in expression of 433 GATA-1 target genes. ChIP results indicated that the TMG treatment decreases the occupancy of GATA-1, OGT, and OGA at the GATA-binding site of the lysosomal protein transmembrane 5 (Laptm5) gene promoter. TMG also reduced the expression of genes involved in differentiation of NB4 and HL60 human myeloid leukemia cells, suggesting that O-GlcNAcylation is involved in the regulation of hematopoietic differentiation. Sustained treatment of G1E-ER4 cells with TMG before differentiation reduced hemoglobin-positive cells and increased stem/progenitor cell surface markers. Our results show that alterations in O-GlcNAcylation disrupt transcriptional programs controlling erythropoietic lineage commitment, suggesting a role for O-GlcNAcylation in regulating hematopoietic cell fate.

| S-EPMC6349094 | biostudies-literature

Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control

Project description:Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control

| PRJNA557313 | ENA

Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control [II]

Project description:Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control [II]

| PRJNA557111 | ENA

Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control [I]

Project description:Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control [I]

| PRJNA555627 | ENA

Notch-HES1 signaling axis controls hemato-endothelial fate decisions of human embyronic and induced pluripotent cells

Project description:Notch signaling regulates several cellular processes including cell fate decisions and proliferation in both invertebrates and mice. However, comparatively less is known about the role of Notch during early human development. Here, we examined the function of Notch signaling during hematopoietic lineage specification from human pluripotent stem cells (hPSCs) of both embryonic and adult fibroblast origin. Using immobilized Notch ligands and siRNA to Notch receptors we have demonstrated that Notch1, but not Notch2 activation, induced HES1 expression and generation of committed hematopoietic progenitors. Using gain and loss of function approaches, this was shown to be attributed to Notch signaling regulation through HES1, that dictated cell fate decisions from bipotent precursors either to the endothelial or hematopoietic lineages at the clonal level. Our study reveals a previously unappreciated role for the Notch pathway during early human hematopoiesis, whereby Notch signaling via HES1 represents a toggle switch of hematopoietic vs. endothelial fate specification. Human pluripotent stem cells (hPSCs) have differentiation potential into three embryonic germ layers including blood. Notch signaling is one of important signaling pathways involved in blood differentiation of hPSCs. Thus, in order to examine the effect of Notch signaling pathways during hematopoietic differentiation of hPSCs, embryoid bodies (EBs) were formed and cultured for 10 days in the combination of cytokines and growth factors (Chadwick, Blood, 2003; 300 ng/ml of SCF, 300 ng/ml of Flt-3L, 10 ng/ml of IL-3, 10 ng/ml of IL-6, and 50 ng/ml of G-CSF) to induce differentiation into blood. Additionally, CD31+CD45- bipotent hemogenic precursors were isolated from day10 hematopoietic EBs (Wang et al., Immunity, 2004)

2013-06-01 | E-GEOD-47466 | biostudies-arrayexpress

Loss of RUNX1 favors mesenchymal stem cells development at the expense of hematopoiesis in hPSC-derived hematopoiesis

Project description:Our data demonstrated an unprecedented role of RUNX1 in regulating hematopoietic and mesenchymal fate decisions in human pluripotent stem cells (hPSC)-derived hematopoiesis

2024-05-17 | GSE232147 | GEO

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions in dictating tissue homeostasis versus tissue homeostasis

2022-10-04 | GSE206458 | GEO

Metabolic reprogramming of innate-like T cell fate and tissue homeostasis by PTEN [scRNA- and scTCR-seq]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions in dictating tissue homeostasis versus fatal autoimmunity

2022-10-04 | GSE179511 | GEO

The dynamics of Atm signalling dictate cellular fate decisions after DNA damage

Project description:DNA damage activates diverse cellular responses â€“ either protective or deleterious â€“that ultimately promote or inhibit proliferation. How the distinct responses conferring crucial cell fate decisions are chosen is unclear. Using a systems approach, we demonstrate that the dynamic features of Atm dependent DNA double-strand break (DSB) signalling response dictate cellular outcome. Combining temporal phosphoproteome and nascent transcriptome analyses after low or high DNA-damage-load, we discovered that some responses, such as Tp53 activation, have an activation threshold and others arise independently of DNA-damage-load. Using DSB repair deficient cells, we show that persistent DSBs alter the kinetics â€“ but not the amplitude â€“ of Atm signalling. Thus, we demonstrate that pathway choices are dictated by the signalling dynamics and hence cell fate decisions are responsive to DNA-damage-load and repair capacity of the cells.

2023-01-18 | PXD013620 | Pride

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