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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk II

ABSTRACT: To determine the physiological roles of zinc in erythroid progenitor cells, cellular zinc was restricted by 50 µM DTPA treatment (a zinc chelator) for 24 hours in differentiating G1E-ER4 cells. G1E-ER4 cells induced for differentiation by beta-estradiol were divided into two groups: control and 50 µM DTPA treatment. A sample from cells untreated with beta-estradiol was also included as an undifferentiated group.

ORGANISM(S): Mus musculus

PROVIDER: GSE310207 | GEO | 2025/11/19

REPOSITORIES: GEO

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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk I

Project description:To determine the effects of heme synthesis inhibition via different pathways in erythroid progenitor cells, heme synthesis was inhibited by 50 µM DTPA treatment (a zinc chelator), 50 µM DFO treatment (a iron chelator), or 0.2 mM succinylacetone (SA, a ALAD inhibitor) for 24 hours in differentiating G1E-ER4 cells. G1E-ER4 Cells were divided into four groups: untreated control, 50 µM DTPA treatment, 50 µM DFO treatment, and 0.2 mM SA. The transcriptome profiles acquired from RNA-seq were compared with those of control cells.

2025-11-19 | GSE310206 | GEO

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Pol2ChIP]

Project description:ChIP-seq of total Pol II in G1E ER4 cell line at time points after mitosis. Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.

2016-06-15 | E-GEOD-83263 | biostudies-arrayexpress

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition [Hist]

Project description:ChIP-seq of H3K27Ac in the G1E-ER4 cell line in prometaphase (nocodazole block), between anaphase-telophase (nocodazole release 40min), and interphase (asynchronous). Nocodazole arrest-release in G1E ER4 cell line under conditions of 13h estradiol treatment.

2016-06-15 | E-GEOD-83255 | biostudies-arrayexpress

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

GATA-1-regulated erythroid microRNAs

Project description:We employed a gene complementation strategy combined with microarray screening to identify miRNAs involved in the formation of erythroid (red blood) cells. To search for GATA-1-regulated erythroid miRNAs, we used the Gata-1– erythroblast line G1E. These cells proliferate in culture as immature erythroid precursors and undergo terminal maturation when GATA-1 activity is restored. G1E-ER4 is a sub-line stably expressing an estrogen-activated form of GATA-1 (GATA-1 fused to the ligand binding domain of the estrogen receptor). Treatment of G1E-ER4 cells with estradiol induces a GATA-1-regulated program of gene expression with concomitant cellular maturation. We used a microarray to evaluate the expression of 292 different miRNAs in G1E-ER4 cells at 0 versus 24 hours after GATA-1 activation. Affymetrix gene expression profiling has previously been deposited (GEO accession no. GSE628). Keywords: microRNA analysis of a cell-line model of erythroid maturation Two condition experiment, 3 replicates each (independently grown and harvested) of untreated and estradiol-treated (24hrs) G1E-ER4 cells, which express an estrogen-responsive form of the GATA-1 transcription factor. Each sample is compared to a common reference sample, comprised of an equal mixture of all 6 experimental samples.

2008-02-05 | E-GEOD-10134 | biostudies-arrayexpress

GATA-1-regulated erythroid microRNAs

2008-02-05 | GSE10134 | GEO

Erythroid differentiation: G1E model

2009-09-10 | GSE18042 | GEO

The mechanistic studies of GATA1 regulation of SREBP2 in G1-ER4 cells

Project description:In our work, we uncovered a critical role for cholesterol homeostasis in terminal erythropoiesis. The master transcriptional factor GATA1 binds to Sterol-regulatory element binding protein 2 (SREBP2) to downregulate cholesterol biosynthesis, leading to a gradual reduction in intracellular cholesterol levels. To reveal genetic interactions and epistatic relations between GATA1 and SREBP2 on depth at the whole genome level, we performed RNA sequencing to analyze the gene expression profiles change between treated with Vehicle or β-estradiol in overexpressing active SREBP2 G1E-ER4 cells.

2022-02-08 | GSE184002 | GEO

Transcription profiling of mouse erythroid differentiation using Gata1 gene-disrupted G1E ER4 clone cells

Project description:Analysis of erythroid differentiation using Gata1 gene-disrupted G1E ER4 clone cells. Estradiol addition activates an ectopically expressed Gata-1-estrogen receptor fusion protein, triggering synchronous differentiation. 30 hour time course corresponds roughly to late burst-forming unit-erythroid stage (t=0 hrs) through orthochromatic erythroblast stage (t=30 hrs). Experiment Overall Design: G1E ER4 cells cultured in G1E medium were treated at 6 time points with estradiol to initiate erythroid differentiation by activating Gata1 transcription factor and total RNAs from treated cells were extracted for microarray experiment. The erythroid differentiation status was confirmed by cell pellet color and expression of microRNA miR451. The design was similar to an earlier studies (Welch, J. J., Watts, J. A., Vakoc, C. R., Yao, Y., Wang, H., Hardison, R. C., Blobel, G. A., Chodosh, L. A., and Weiss, M. J. (2004)). Global regulation of erythroid gene expression by transcription factor GATA-1. Blood 104, 3136-3147), except that a more recent version of Affymetric chip was used to acheive greater transcriptome coverage.

2009-09-18 | E-GEOD-18042 | biostudies-arrayexpress

BRD2 cooperates with CTCF to enforce transcriptional and architectural boundaries

Project description:BET (bromodomain and extraterminal motif) proteins are pharmacologic targets for the treatment of diverse diseases, yet the roles of individual BET family members remain unclear. We find that BRD2 colocalizes with the architectural/insulator protein CCCTC-binding factor (CTCF) genome-wide. To test a role for BRD2 in chromatin architecture we performed HiC in uninduced G1E-ER4 cells (-GATA1), and compared it to HiC in BRD2-depleted G1E-ER4 cells

2017-03-31 | GSE95476 | GEO

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