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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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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: Not available

| S-EPMC6349094 | biostudies-literature

NOTCH-driven oscillations control cell fate decisions during intestinal homeostasis

Project description:NOTCH-driven oscillations control cell fate decisions during intestinal homeostasis

| PRJNA1156195 | ENA

Bcl11a orchestrates multilineage integrity in aging hematopoiesis by regulating multipotent progenitor fate decisions

Project description:Bcl11a orchestrates multilineage integrity in aging hematopoiesis by regulating multipotent progenitor fate decisions

| PRJNA1406321 | ENA

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

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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

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

Bcl11a orchestrates multilineage integrity in aging hematopoiesis by regulating multipotent progenitor fate decisions [CUT&Tag]

Project description:Bcl11a orchestrates multilineage integrity in aging hematopoiesis by regulating multipotent progenitor fate decisions [CUT&Tag]

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Bcl11a orchestrates multilineage integrity in aging hematopoiesis by regulating multipotent progenitor fate decisions [ATAC-seq]

Project description:Bcl11a orchestrates multilineage integrity in aging hematopoiesis by regulating multipotent progenitor fate decisions [ATAC-seq]

| PRJNA1405575 | ENA

DNMT3A regulates megakaryocyte-biased HSC fate decisions

Project description:We characterized the role of the DNA methyltransferase DNMT3A in the fate decisions of murine megakaryocyte-biased HSCs and in the differentiation of megakaryocytes and platelets. In this experiment, we isolated washed platelets from 4 WT and 4 Dnmt3a+/– germline mice (2 males and 2 females per group) and subjected them to proteomic analysis by mass-spectrometry. We sought to identify changes at the protein level that occur in platelets due to aberrant DNA methylation during the differentiation of upstream hematopoietic cells.

2025-06-09 | PXD055265 | Pride

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